G
G:I ratio
Genes/genetics
GIP - see Incretins
GLP-1 - see Incretins
Glycemic index/load
Glucagon
Glucocorticoids - see Corticosteroids
Glucosamine
Glucose
GLUTs (glucose transporters)
Glyburide
Goat's Rue
Grass
Growth hormone
Genes/genetics
GIP - see Incretins
GLP-1 - see Incretins
Glycemic index/load
Glucagon
Glucocorticoids - see Corticosteroids
Glucosamine
Glucose
GLUTs (glucose transporters)
Glyburide
Goat's Rue
Grass
Growth hormone
G:I ratio
IR calculator - enter your horse's glucose and insulin blood results and the G:I ratio, RISQI, MIRG and IR status is calculated for you.
G:I over 10:1 = normal
G:I between 4.5:1 and 10:1 = compensated IR
G:I less than 4.5:1 = severe IR/high laminitis risk
G:I over 10:1 = normal
G:I between 4.5:1 and 10:1 = compensated IR
G:I less than 4.5:1 = severe IR/high laminitis risk
Genes/genetics
Galantino-Homer H, Brooks SA
Genetics and Signaling Pathways of Laminitis
Vet Clin North Am Equine Pract. Aug 2020;36(2):379-394. doi: 10.1016/j.cveq.2020.04.001
Norton E, McCue M
Genetics of Equine Endocrine and Metabolic Disease
Vet Clin North Am Equine Pract. published online 10 June 2020; S0749-0739(20)30022-5. doi:10.1016/j.cveq.2020.03.011
Norton E, Schultz N, Geor R, McFarlane D, Mickelson J, McCue M
Genome-Wide Association Analyses of Equine Metabolic Syndrome Phenotypes in Welsh Ponies and Morgan Horses
Genes (Basel)6 Nov 2019; 10(11):893. doi: 10.3390/genes10110893
Norton EM, Schultz NE, Rendahl AK, Mcfarlane D, Geor RJ, Mickelson JR, McCue ME
Heritability of metabolic traits associated with equine metabolic syndrome in Welsh ponies and Morgan horses
Equine Vet J. 2019 Jul;51(4):475-480. doi: 10.1111/evj.13053. Epub 2018 Dec 15
The paper found evidence of a genetic contribution to key phenotypes associated with EMS, but concluded that "attempting to eliminate EMS through breeding is not feasible, nor recommended, as it would have undesired consequences including decreasing genetic diversity within breeds". However, genetic testing would help to assess a horse's risk of developing EMS, alongside environmental risk factors, which could help to identify horses that might need closer monitoring and benefit from early environmental modification, and those with a higher genetic risk for EMS that might need stricter management. Genetic testing could also guide responsible breeding, and avoid breeding horses with a high genetic risk for EMS together.
Norton EM, Avila F, Schultz NE, Mickelson JR, Geor RJ, McCue ME
Evaluation of an HMGA2 variant for pleiotropic effects on height and metabolic traits in ponies
J Vet Intern Med. 2019 Jan 21. doi: 10.1111/jvim.15403. [Epub ahead of print]
Lewis SL, Holl HM, Streeter C, Posbergh C, Schanbacher BJ, Place NJ, Mallicote MF, Long MT, Brooks SA
Genomewide association study reveals a risk locus for equine metabolic syndrome in the Arabian horse
J Anim Sci. 2017 Mar;95(3):1071-1079. doi: 10.2527/jas.2016.1221
Risk Factors for Equine Metabolic Syndrome - Dr Nichol Schultz 29 Jan 2013
Galantino-Homer H, Brooks SA
Genetics and Signaling Pathways of Laminitis
Vet Clin North Am Equine Pract. Aug 2020;36(2):379-394. doi: 10.1016/j.cveq.2020.04.001
Norton E, McCue M
Genetics of Equine Endocrine and Metabolic Disease
Vet Clin North Am Equine Pract. published online 10 June 2020; S0749-0739(20)30022-5. doi:10.1016/j.cveq.2020.03.011
Norton E, Schultz N, Geor R, McFarlane D, Mickelson J, McCue M
Genome-Wide Association Analyses of Equine Metabolic Syndrome Phenotypes in Welsh Ponies and Morgan Horses
Genes (Basel)6 Nov 2019; 10(11):893. doi: 10.3390/genes10110893
Norton EM, Schultz NE, Rendahl AK, Mcfarlane D, Geor RJ, Mickelson JR, McCue ME
Heritability of metabolic traits associated with equine metabolic syndrome in Welsh ponies and Morgan horses
Equine Vet J. 2019 Jul;51(4):475-480. doi: 10.1111/evj.13053. Epub 2018 Dec 15
The paper found evidence of a genetic contribution to key phenotypes associated with EMS, but concluded that "attempting to eliminate EMS through breeding is not feasible, nor recommended, as it would have undesired consequences including decreasing genetic diversity within breeds". However, genetic testing would help to assess a horse's risk of developing EMS, alongside environmental risk factors, which could help to identify horses that might need closer monitoring and benefit from early environmental modification, and those with a higher genetic risk for EMS that might need stricter management. Genetic testing could also guide responsible breeding, and avoid breeding horses with a high genetic risk for EMS together.
Norton EM, Avila F, Schultz NE, Mickelson JR, Geor RJ, McCue ME
Evaluation of an HMGA2 variant for pleiotropic effects on height and metabolic traits in ponies
J Vet Intern Med. 2019 Jan 21. doi: 10.1111/jvim.15403. [Epub ahead of print]
Lewis SL, Holl HM, Streeter C, Posbergh C, Schanbacher BJ, Place NJ, Mallicote MF, Long MT, Brooks SA
Genomewide association study reveals a risk locus for equine metabolic syndrome in the Arabian horse
J Anim Sci. 2017 Mar;95(3):1071-1079. doi: 10.2527/jas.2016.1221
Risk Factors for Equine Metabolic Syndrome - Dr Nichol Schultz 29 Jan 2013
Glycemic index/load
The glycemic response is the body's blood glucose (and insulin) response to a meal or food eaten.
The glycemic index (GI) is a number associated with a feed that reflects that feed's affect on blood glucose in comparison to a standard food (e.g. glucose/white bread in humans, oats in horses) - the higher the GI, the more blood sugar levels increase after the food is eaten. The GI does not take into account how much of the feed is eaten.
The glycemic load (GL) takes into account how much of the feed is eaten, and is a factor of the amount of carbohydrate in the feed x the feed's GI.
The glycemic index and load are used in human nutrition to help formulate diets for diabetics that do not adversely raise blood sugar levels.
The glycemic index of horse feeds should be useful because sugar and starch digestion and glucose metabolism in horses is similar to humans. However, although research has been carried out on horses, a lack of standardization between experiments and high variability in results has limited the use of glycemic indices/load in horses.
Rodiek AV, Stull CL
Glycemic Index of Ten Common Horse Feeds
Journal of Equine Veterinary Science May 2007 Volume 27, Issue 5, Pages 205–211
6 healthy Quarter Horse mares were fed 10 feeds, given in quantities to provide 4 Mcal DE per meal of that feed, and blood collected for 300 minutes after feeding and tested for glucose concentration.
Vervuert I, Coenen M
Factors affecting glycaemic index of feeds for horses
Proceedings of the 3rd European Equine Nutrition & Health Congress, Hannover, March 2006
Kronfeld D, Rodiek A, Stull C
Glycemic indices, glycemic loads, and glycemic dietetics
JEVS September 2004Volume 24, Issue 9, Pages 399–404 (DeepDyve)
Glycemic index/load in humans
www.glycemicindex.com - the official website for the glycemic index and international GI database based in the Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders and Charles Perkins Centre at the University of Sydney.
See Who said "stop the carrots"? for GI and GL figures for raw carrots.
The glycemic response is the body's blood glucose (and insulin) response to a meal or food eaten.
The glycemic index (GI) is a number associated with a feed that reflects that feed's affect on blood glucose in comparison to a standard food (e.g. glucose/white bread in humans, oats in horses) - the higher the GI, the more blood sugar levels increase after the food is eaten. The GI does not take into account how much of the feed is eaten.
The glycemic load (GL) takes into account how much of the feed is eaten, and is a factor of the amount of carbohydrate in the feed x the feed's GI.
The glycemic index and load are used in human nutrition to help formulate diets for diabetics that do not adversely raise blood sugar levels.
The glycemic index of horse feeds should be useful because sugar and starch digestion and glucose metabolism in horses is similar to humans. However, although research has been carried out on horses, a lack of standardization between experiments and high variability in results has limited the use of glycemic indices/load in horses.
Rodiek AV, Stull CL
Glycemic Index of Ten Common Horse Feeds
Journal of Equine Veterinary Science May 2007 Volume 27, Issue 5, Pages 205–211
6 healthy Quarter Horse mares were fed 10 feeds, given in quantities to provide 4 Mcal DE per meal of that feed, and blood collected for 300 minutes after feeding and tested for glucose concentration.
Vervuert I, Coenen M
Factors affecting glycaemic index of feeds for horses
Proceedings of the 3rd European Equine Nutrition & Health Congress, Hannover, March 2006
Kronfeld D, Rodiek A, Stull C
Glycemic indices, glycemic loads, and glycemic dietetics
JEVS September 2004Volume 24, Issue 9, Pages 399–404 (DeepDyve)
Glycemic index/load in humans
www.glycemicindex.com - the official website for the glycemic index and international GI database based in the Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders and Charles Perkins Centre at the University of Sydney.
See Who said "stop the carrots"? for GI and GL figures for raw carrots.
Glucagon
Newkirk KM, Ehrensing G, Odoi A, Boston RC, Frank N
Immunohistochemical expression of insulin, glucagon, and somatostatin in pancreatic islets of horses with and without insulin resistance
Am J Vet Res. 2018 Feb;79(2):191-198. doi: 10.2460/ajvr.79.2.191
"Results suggested that, in insulin-resistant horses, insulin secretion was not increased but glucagon production might be downregulated as a compensatory response to hyperinsulinemia."
Newkirk KM, Ehrensing G, Odoi A, Boston RC, Frank N
Immunohistochemical expression of insulin, glucagon, and somatostatin in pancreatic islets of horses with and without insulin resistance
Am J Vet Res. 2018 Feb;79(2):191-198. doi: 10.2460/ajvr.79.2.191
"Results suggested that, in insulin-resistant horses, insulin secretion was not increased but glucagon production might be downregulated as a compensatory response to hyperinsulinemia."
Glucosamine
Glucosamine is often recommended as a joint supplement, but is it effective, and is it safe for insulin resistant horses?
NB laminitic horses are commonly thought to be suffering from joint stiffness or pain from arthritis, when in fact it is low grade laminitis or foot pain from chronic laminitis that is causing the horse to move in an stiff manner. Nerve blocking the feet may help decide whether the pain is from laminitis or arthritis.
Glucosamine efficacy
Proceedings of the 47th British Equine Veterinary Association Congress BEVA Sep. 10 – 13, 2008
Update on medical treatment of joint disease
Sheila Laverty
Glucosamine and Insulin Resistance
TLS is not aware of any studies in horses. Studies in other species:
Some research has found that glucosamine causes or worsens insulin resistance:
Am J Med Sci. 2007 Jun;333(6):333-9 (PubMed)
Oral glucosamine in doses used to treat osteoarthritis worsens insulin resistance
Pham T, Cornea A, Blick KE, Jenkins A, Scofield RH
"Conclusion: Notwithstanding its efficacy remaining in question, glucosamine is widely used as treatment for osteoarthritis, which is a condition associated with both obesity and type 2 diabetes mellitus. Our data indicate that persons with underlying poorer insulin sensitivity are at risk for worsening insulin resistance and vascular function with the use of glucosamine in doses used to treat osteoarthritis."
Diabetes Obes Metab. 2004 Jul;6(4):293-8 (PubMed)
Glucosamine-induced insulin resistance in L6 muscle cells
Bailey CJ, Turner SL
Muscle cells incubated with high levels of glucosamine had reduced glucose uptake:
"Conclusion: Glucosamine decreased insulin-stimulated glucose uptake by L6 muscle cells, providing a potential model of insulin resistance with similarities to glucose toxicity. Insulin resistance induced by glucosamine was not reversed by three agents (metformin, peroxovanadium and d-pinitol) known to enhance or partially mimic the effects of insulin."
Some research has found that glucosamine at recommended doses does not appear to have adverse effects on glucose metabolism:
Diabetes Care June 2003 vol. 26 no. 6 1941-1942
The Effect of Oral Glucosamine Sulfate on Insulin Sensitivity in Human Subjects
Yu JG, Boies SM, Olefsky JM
And some research has found mixed results:
Osteoarthritis Cartilage. 2011 Apr;19(4):375-80 (PubMed)
The effect of glucosamine on glucose metabolism in humans: a systematic review of the literature
Dostrovsky NR, Towheed TE, Hudson RW, Anastassiades TP"Four of the studies found decreased insulin sensitivity or increased fasting glucose in subjects taking glucosamine. Three of these were clinical studies using oral glucosamine. Studies that included subjects with baseline impaired glucose tolerance or insulin resistance were more likely to detect an effect on glucose metabolism than studies without such subjects."
Ann Rheum Dis. 2007 February; 66(2): 260–262
Effects of oral glucosamine sulphate on serum glucose and insulin during an oral glucose tolerance test of subjects with osteoarthritis
B A Biggee, C M Blinn, M Nuite, J E Silbert, and T E McAlindon
A single dose of glucosamine sulphate had no effect on insulin levels but did appear to affect glucose levels in patients with glucose intolerance.
TLS commment: Research has shown that glucosamine can produce/increase insulin resistance, but some studies have found no effect on glucose or insulin. So best to be cautious, but not necessarily avoid using it with an insulin resistant horse, as long as the insulin resistance is not uncontrolled. If the horse is already having glucosamine with no obvious ill effects, it's probably ok to continue. If the horse hasn't had glucosamine before and you want to use it for joint problems, introduce carefully, monitor closely and stop giving it at the first sign of any unexplained foot pain/sensitivity. In all cases with an insulin resistant horse, best to check insulin (and glucose) levels regularly.
Glucosamine is often recommended as a joint supplement, but is it effective, and is it safe for insulin resistant horses?
NB laminitic horses are commonly thought to be suffering from joint stiffness or pain from arthritis, when in fact it is low grade laminitis or foot pain from chronic laminitis that is causing the horse to move in an stiff manner. Nerve blocking the feet may help decide whether the pain is from laminitis or arthritis.
Glucosamine efficacy
Proceedings of the 47th British Equine Veterinary Association Congress BEVA Sep. 10 – 13, 2008
Update on medical treatment of joint disease
Sheila Laverty
Glucosamine and Insulin Resistance
TLS is not aware of any studies in horses. Studies in other species:
Some research has found that glucosamine causes or worsens insulin resistance:
Am J Med Sci. 2007 Jun;333(6):333-9 (PubMed)
Oral glucosamine in doses used to treat osteoarthritis worsens insulin resistance
Pham T, Cornea A, Blick KE, Jenkins A, Scofield RH
"Conclusion: Notwithstanding its efficacy remaining in question, glucosamine is widely used as treatment for osteoarthritis, which is a condition associated with both obesity and type 2 diabetes mellitus. Our data indicate that persons with underlying poorer insulin sensitivity are at risk for worsening insulin resistance and vascular function with the use of glucosamine in doses used to treat osteoarthritis."
Diabetes Obes Metab. 2004 Jul;6(4):293-8 (PubMed)
Glucosamine-induced insulin resistance in L6 muscle cells
Bailey CJ, Turner SL
Muscle cells incubated with high levels of glucosamine had reduced glucose uptake:
"Conclusion: Glucosamine decreased insulin-stimulated glucose uptake by L6 muscle cells, providing a potential model of insulin resistance with similarities to glucose toxicity. Insulin resistance induced by glucosamine was not reversed by three agents (metformin, peroxovanadium and d-pinitol) known to enhance or partially mimic the effects of insulin."
Some research has found that glucosamine at recommended doses does not appear to have adverse effects on glucose metabolism:
Diabetes Care June 2003 vol. 26 no. 6 1941-1942
The Effect of Oral Glucosamine Sulfate on Insulin Sensitivity in Human Subjects
Yu JG, Boies SM, Olefsky JM
And some research has found mixed results:
Osteoarthritis Cartilage. 2011 Apr;19(4):375-80 (PubMed)
The effect of glucosamine on glucose metabolism in humans: a systematic review of the literature
Dostrovsky NR, Towheed TE, Hudson RW, Anastassiades TP"Four of the studies found decreased insulin sensitivity or increased fasting glucose in subjects taking glucosamine. Three of these were clinical studies using oral glucosamine. Studies that included subjects with baseline impaired glucose tolerance or insulin resistance were more likely to detect an effect on glucose metabolism than studies without such subjects."
Ann Rheum Dis. 2007 February; 66(2): 260–262
Effects of oral glucosamine sulphate on serum glucose and insulin during an oral glucose tolerance test of subjects with osteoarthritis
B A Biggee, C M Blinn, M Nuite, J E Silbert, and T E McAlindon
A single dose of glucosamine sulphate had no effect on insulin levels but did appear to affect glucose levels in patients with glucose intolerance.
TLS commment: Research has shown that glucosamine can produce/increase insulin resistance, but some studies have found no effect on glucose or insulin. So best to be cautious, but not necessarily avoid using it with an insulin resistant horse, as long as the insulin resistance is not uncontrolled. If the horse is already having glucosamine with no obvious ill effects, it's probably ok to continue. If the horse hasn't had glucosamine before and you want to use it for joint problems, introduce carefully, monitor closely and stop giving it at the first sign of any unexplained foot pain/sensitivity. In all cases with an insulin resistant horse, best to check insulin (and glucose) levels regularly.
Glucose
Glucose conversion between mmol/L and mg/dL
glucose in mmol/L x 18 = glucose in mg/dL
glucose in mg/dL ÷ 18 = glucose in mmol/L
SydPath Unit Conversion Table will do the conversion for you
Glucose measured in whole blood is around 12% lower than glucose measured in plasma - www.diabetes.co.uk has a whole blood/plasma conversion
Some normal reference ranges:
Liphook Equine Hospital: 3.2 - 6.9 mmol/L
Cornell 71 - 113 mg/dL
MSU 4.3 - 6.9 mmol/L
Beaufort Cottage Laboratories (Rossdales) adult non-TB horses 4.3 - 5.5 mmol/L
New Bolton Centre Field Service Dept. 72 - 114 mg/dL
Manual of Equine Practice 1999 Reuben J Rose, David R Hodgson 4.1 - 6.4 mmol/L (75 - 115 mg/dL)
With insulin resistance/EMS blood glucose levels are normal.
With diabetes mellitus blood glucose levels are above normal - hyperglycaemia
Standard protocol for testing glucose (from plasma) - but always follow the protocol of the testing laboratory
Starve for 6 hours
(For diagnosis of Insulin resistance, collect blood for glucose and insulin testing at the same time)
Collect into oxalate-fluoride (grey-topped) tube
Centrifuge or allow to separate by gravity
Decant off the plasma into another tube
Despatch to lab (can be chilled/included in chiller pack as long as the plasma has been separated off)
Blood glucose is raised by feeding, stress, excitement and exercise, and is influenced by intestinal absorption, liver production, hormones and use by tissues.
Hyperglycaemia can result from insulin deficiency, reduced use of glucose by tissues, increased gluconeogenesis and increased glycogenolysis (both the latter are increased by TRH, GH, glucocorticoids, glucagon and catecholamines). Endotoxaemia/septicaemia and shock may also cause hyperglycaemia.
"Glucose is reduced in stored whole blood due to ex vivo glycolysis. This is minimised by the use of potassium oxalate/sodium fluoride, which acts as a preservative. Recent work suggests that glucose decreases using these tubes, but it is not as marked a decrease in comparison to plain serum tubes (Rendle et al 2009). Thus, it is appropriate to use potassium oxalate/sodium fluoride (grey topped) tubes to transport whole blood for glucose measurement." Liphook Equine Hospital - Time-dependent Artifacts in Clinical Pathology
Glucose - Cornell EClinPath
Can high glucose cause laminitis in healthy horses?
In the study below, glucose (50% dextrose) was given IV at a rate of 0.68 ml/kg/h for 48 hours to insulin sensitive (i.e. not insulin resistant) horses. The horses developed glycosuria, hyperglycaemia (10.7 +/- 0.78 mmol/L) and hyperinsulinaemia (208 +/- 26.1 µIU/mL), and all of the horses developed histopathological evidence of laminitis in at least one foot, although none became lame.
Vet J. 2011 Aug 26
Continuous intravenous infusion of glucose induces endogenous hyperinsulinaemia and lamellar histopathology in Standardbred horses
de Laat M, Sillence M, McGowan C, Pollitt C
"Combined with earlier studies, the results showed that laminitis may be induced by either insulin alone or a combination of insulin and glucose, but that it is unlikely to be due to a glucose overload mechanism."
Hyperglycaemia - glucose concentration is greater than the laboratory reference range.
Hyperglycemia - Cornell
Hyperglycaemia can occur post prandially (after eating), particularly after eating foods containing glucose/dextrose, other sugars and starch.
Hyperglycaemia can also be caused by:
Glucose and insulin dynamics associated with continuous infusion of dextrose or dextrose and insulin in healthy and endotoxin-exposed horses
Janet Han - MSc thesis 2008
See Diabetes mellitus
Glucosuria
Hyperglycaemia can lead to glucosuria - glucose in the urine. Normal/healthy horse urine does not contain glucose.
In the kidneys, plasma from the blood is filtered in the renal tubules. In a healthy horse, all glucose is reabsorbed in the proximal convoluted tubules, so glucose never gets into the urine. However reabsorption of glucose depends on secondary active transport to move glucose from the renal tubules back into the blood. These transporters can become saturated, i.e. they are all occupied at a certain threshold, so when concentrations of glucose exceed the renal threshold for glucose, some glucose will be unable to be reabsorbed and will be excreted from the body in the urine. The glucose in what will become urine "holds" water, preventing water from being reabsorbed back into the blood, causing the volume of urine to increase, and therefore the horse has to drink more - so leading to PU/PD (polyuria/polydipsia).
The renal threshold for glucose in adult horses, leading to glucosuria, varies considerably according to the source:
11 mmol/l or 200 mg/dl - Equine Clinical Medicine, Surgery and Reproduction - Graham Munroe, Scott Weese
150 - 160 mg/dL - AHDC (Cornell)
160 - 180 mg/dL - Current Therapy in Equine Medicine Ch. 88
175 mg/dL (9.7 mmol/L) Schott HC II: Examination of the Urinary System. In Equine Internal Medicine. 2nd edition. Edited by Reed SM, Bayly WM, Sellon DC. Missouri, USA: Saunders; 2004:1200-1210. (Referenced by Arosalo et a. 2007).
180 - 200 mg/dL - Blackwell's five-minute veterinary consult
> 180 mg/dL - The Merck Veterinary Manual, The Equine Hospital Manual
200 - 220 mg/dL - Current Therapy in Equine Medicine Ch. 22
The renal threshold for glucose is higher in foals.
Glucose in the urine can be measured with a dipstick.
glucose in mmol/L x 18 = glucose in mg/dL
glucose in mg/dL ÷ 18 = glucose in mmol/L
SydPath Unit Conversion Table will do the conversion for you
Glucose measured in whole blood is around 12% lower than glucose measured in plasma - www.diabetes.co.uk has a whole blood/plasma conversion
Some normal reference ranges:
Liphook Equine Hospital: 3.2 - 6.9 mmol/L
Cornell 71 - 113 mg/dL
MSU 4.3 - 6.9 mmol/L
Beaufort Cottage Laboratories (Rossdales) adult non-TB horses 4.3 - 5.5 mmol/L
New Bolton Centre Field Service Dept. 72 - 114 mg/dL
Manual of Equine Practice 1999 Reuben J Rose, David R Hodgson 4.1 - 6.4 mmol/L (75 - 115 mg/dL)
With insulin resistance/EMS blood glucose levels are normal.
With diabetes mellitus blood glucose levels are above normal - hyperglycaemia
Standard protocol for testing glucose (from plasma) - but always follow the protocol of the testing laboratory
Starve for 6 hours
(For diagnosis of Insulin resistance, collect blood for glucose and insulin testing at the same time)
Collect into oxalate-fluoride (grey-topped) tube
Centrifuge or allow to separate by gravity
Decant off the plasma into another tube
Despatch to lab (can be chilled/included in chiller pack as long as the plasma has been separated off)
Blood glucose is raised by feeding, stress, excitement and exercise, and is influenced by intestinal absorption, liver production, hormones and use by tissues.
Hyperglycaemia can result from insulin deficiency, reduced use of glucose by tissues, increased gluconeogenesis and increased glycogenolysis (both the latter are increased by TRH, GH, glucocorticoids, glucagon and catecholamines). Endotoxaemia/septicaemia and shock may also cause hyperglycaemia.
"Glucose is reduced in stored whole blood due to ex vivo glycolysis. This is minimised by the use of potassium oxalate/sodium fluoride, which acts as a preservative. Recent work suggests that glucose decreases using these tubes, but it is not as marked a decrease in comparison to plain serum tubes (Rendle et al 2009). Thus, it is appropriate to use potassium oxalate/sodium fluoride (grey topped) tubes to transport whole blood for glucose measurement." Liphook Equine Hospital - Time-dependent Artifacts in Clinical Pathology
Glucose - Cornell EClinPath
Can high glucose cause laminitis in healthy horses?
In the study below, glucose (50% dextrose) was given IV at a rate of 0.68 ml/kg/h for 48 hours to insulin sensitive (i.e. not insulin resistant) horses. The horses developed glycosuria, hyperglycaemia (10.7 +/- 0.78 mmol/L) and hyperinsulinaemia (208 +/- 26.1 µIU/mL), and all of the horses developed histopathological evidence of laminitis in at least one foot, although none became lame.
Vet J. 2011 Aug 26
Continuous intravenous infusion of glucose induces endogenous hyperinsulinaemia and lamellar histopathology in Standardbred horses
de Laat M, Sillence M, McGowan C, Pollitt C
"Combined with earlier studies, the results showed that laminitis may be induced by either insulin alone or a combination of insulin and glucose, but that it is unlikely to be due to a glucose overload mechanism."
Hyperglycaemia - glucose concentration is greater than the laboratory reference range.
Hyperglycemia - Cornell
Hyperglycaemia can occur post prandially (after eating), particularly after eating foods containing glucose/dextrose, other sugars and starch.
Hyperglycaemia can also be caused by:
- Severe illness e.g. colic* - Association between Hyperglycemia and Survival in 228 Horses with Acute Gastrointestinal Disease
- Diabetes Mellitus
- PPID
- Excessive endogenous or exogenous glucocorticoids
- Stress (epinephrine/norepinephrine)
- Transient hyperglycaemia can be caused by some sedatives , particularly xylazine and detomidine (source: Blackwell's five-minute veterinary consult 2008 p344), e.g. Dormosedan
Glucose and insulin dynamics associated with continuous infusion of dextrose or dextrose and insulin in healthy and endotoxin-exposed horses
Janet Han - MSc thesis 2008
See Diabetes mellitus
Glucosuria
Hyperglycaemia can lead to glucosuria - glucose in the urine. Normal/healthy horse urine does not contain glucose.
In the kidneys, plasma from the blood is filtered in the renal tubules. In a healthy horse, all glucose is reabsorbed in the proximal convoluted tubules, so glucose never gets into the urine. However reabsorption of glucose depends on secondary active transport to move glucose from the renal tubules back into the blood. These transporters can become saturated, i.e. they are all occupied at a certain threshold, so when concentrations of glucose exceed the renal threshold for glucose, some glucose will be unable to be reabsorbed and will be excreted from the body in the urine. The glucose in what will become urine "holds" water, preventing water from being reabsorbed back into the blood, causing the volume of urine to increase, and therefore the horse has to drink more - so leading to PU/PD (polyuria/polydipsia).
The renal threshold for glucose in adult horses, leading to glucosuria, varies considerably according to the source:
11 mmol/l or 200 mg/dl - Equine Clinical Medicine, Surgery and Reproduction - Graham Munroe, Scott Weese
150 - 160 mg/dL - AHDC (Cornell)
160 - 180 mg/dL - Current Therapy in Equine Medicine Ch. 88
175 mg/dL (9.7 mmol/L) Schott HC II: Examination of the Urinary System. In Equine Internal Medicine. 2nd edition. Edited by Reed SM, Bayly WM, Sellon DC. Missouri, USA: Saunders; 2004:1200-1210. (Referenced by Arosalo et a. 2007).
180 - 200 mg/dL - Blackwell's five-minute veterinary consult
> 180 mg/dL - The Merck Veterinary Manual, The Equine Hospital Manual
200 - 220 mg/dL - Current Therapy in Equine Medicine Ch. 22
The renal threshold for glucose is higher in foals.
Glucose in the urine can be measured with a dipstick.
GLUTs (Glucose Transporters)
de Laat MA, Clement CK, Sillence MN, McGowan CM, Pollitt CC, Lacombe VA
The impact of prolonged hyperinsulinaemia on glucose transport in equine skeletal muscle and digital lamellae
Equine Vet J. 2014 Jul 4
Lacombe VA
Expression and regulation of facilitative glucose transporters in equine insulin-sensitive tissue: from physiology to pathology
ISRN Vet Sci. 2014 Mar 4;2014:409547
Waller AP, Huettner L, Kohler K, Lacombe VA
Novel link between inflammation and impaired glucose transport during equine insulin resistance
Vet Immunol Immunopathol. 2012 Oct 15;149(3-4):208-15
Waller AP, Burns TA, Mudge MC, Belknap JK, Lacombe VA
Insulin resistance selectively alters cell-surface glucose transporters but not their total protein expression in equine skeletal muscleJ Vet Intern Med. 2011 Mar-Apr;25(2):315-21
Pflugers Arch - Eur J Physiol (2009) 458:419–430
Adaptive response of equine intestinal Na+/glucose co-transporter (SGLT1) to an increase in dietary soluble carbohydrate
Dyer J, Al-Rammahi M, Waterfall L, Salmon KSH, Geor RJ, Bouré L, Barrie Edwards G, Proudman CJ, Shirazi-Beechey SP
de Laat MA, Clement CK, Sillence MN, McGowan CM, Pollitt CC, Lacombe VA
The impact of prolonged hyperinsulinaemia on glucose transport in equine skeletal muscle and digital lamellae
Equine Vet J. 2014 Jul 4
Lacombe VA
Expression and regulation of facilitative glucose transporters in equine insulin-sensitive tissue: from physiology to pathology
ISRN Vet Sci. 2014 Mar 4;2014:409547
Waller AP, Huettner L, Kohler K, Lacombe VA
Novel link between inflammation and impaired glucose transport during equine insulin resistance
Vet Immunol Immunopathol. 2012 Oct 15;149(3-4):208-15
Waller AP, Burns TA, Mudge MC, Belknap JK, Lacombe VA
Insulin resistance selectively alters cell-surface glucose transporters but not their total protein expression in equine skeletal muscleJ Vet Intern Med. 2011 Mar-Apr;25(2):315-21
Pflugers Arch - Eur J Physiol (2009) 458:419–430
Adaptive response of equine intestinal Na+/glucose co-transporter (SGLT1) to an increase in dietary soluble carbohydrate
Dyer J, Al-Rammahi M, Waterfall L, Salmon KSH, Geor RJ, Bouré L, Barrie Edwards G, Proudman CJ, Shirazi-Beechey SP
Glyburide
Glyburide is a sulfonylurea, prescribed for humans with type 2 diabetes to lower blood glucose levels by increasing insulin production from the pancreas. Many side effects and interactions with other drugs are listed (for humans).
See: Glyburide - RxList
Johnson PJ, Scotty NC, Wiedmeyer C, Messer NT, Kreeger JM.
Diabetes mellitus in a domesticated Spanish mustang.
J Am Vet Med Assoc. 2005 Feb 15;226(4):584-8, 542. doi: 10.2460/javma.2005.226.584. PMID: 15742701.
An 18 year old Spanish Mustang mare had progressive weight loss, hyperglycemia and glycosuria. PPID was ruled out with a dexamethasone suppression test. Serum insulin and plasma C-peptide concentrations were low, suggesting that the high blood glucose was due to reduced insulin secretion from the pancreas. Giving IV insulin only slightly decreased blood glucose levels, suggesting that the action of insulin was impaired. Within 5 hours of giving a combination of glyburide and metformin, blood glucose levels returned to normal. The horse was euthanized [so information about long-term use of these drugs is not available from this research]. Post mortem examination showed reduced beta-cells in the pancreas. Pancreatic beta-cell failure is rare, but may contribute to the development of diabetes mellitus in horses.
Glyburide is a sulfonylurea, prescribed for humans with type 2 diabetes to lower blood glucose levels by increasing insulin production from the pancreas. Many side effects and interactions with other drugs are listed (for humans).
See: Glyburide - RxList
Johnson PJ, Scotty NC, Wiedmeyer C, Messer NT, Kreeger JM.
Diabetes mellitus in a domesticated Spanish mustang.
J Am Vet Med Assoc. 2005 Feb 15;226(4):584-8, 542. doi: 10.2460/javma.2005.226.584. PMID: 15742701.
An 18 year old Spanish Mustang mare had progressive weight loss, hyperglycemia and glycosuria. PPID was ruled out with a dexamethasone suppression test. Serum insulin and plasma C-peptide concentrations were low, suggesting that the high blood glucose was due to reduced insulin secretion from the pancreas. Giving IV insulin only slightly decreased blood glucose levels, suggesting that the action of insulin was impaired. Within 5 hours of giving a combination of glyburide and metformin, blood glucose levels returned to normal. The horse was euthanized [so information about long-term use of these drugs is not available from this research]. Post mortem examination showed reduced beta-cells in the pancreas. Pancreatic beta-cell failure is rare, but may contribute to the development of diabetes mellitus in horses.
Goat's Rue
Goat's Rue or French lilac (Galega officinalis) contains the active ingredients guanidine and galegine (isoamylene guanidine), which decrease blood sugar and were used in the past to treat diabetes. The plant's hypoglycaemic properties led to the synthesis of metformin, a biguanide compound, because the plant itself was considered too toxic for clinical use. Both guanadine and galegine are toxic, and may cause liver and kidney damage, low blood pressure, ataxia, seizures and lactic acidosis.
The questions to be asked are:
Is Goat's Rue toxic to horses?
Does Goat's Rue help horses with EMS by increasing insulin sensitivity?
Toxicity
The FDA Poisonous Plant Database has 42 listings for Goat's Rue/Gelaga officinalis, mostly relating to the poisoning of sheep.
Veterinary Toxicology: Basic and Clinical Principles - Ramesh Chandra Gupta 2012 p 1087
Galegine decreases blood pressure and paralyses the central nervous system. Poisoning generally affects sheep but cattle have been poisoned. Goat's Rue is bitter and poisoning usually follows the consumption of hay or freshly cut fodder.
Symptoms (hydrothorax) appear 12-24 hours after ingestion, leading to death within hours.
J Ethnopharmacol. 2008 Feb 28;116(1):21-6. Epub 2007 Oct 30
Acute and subchronic oral toxicity of Galega officinalis in rats
Rasekh HR, Nazari P, Kamli-Nejad M, Hosseinzadeh L
"sinusoidal congestion in liver and alveolar hemorrhage was observed"... suggesting that "liver and lung could serve as target organs in oral toxicity of this plant".
Hypoglycaemic/insulin sensitising properties
Goatsrue (Galega officinalis) Seed Biology, Control, and Toxicity
Michelle Oldham MSc Thesis Utah State University 2008
P 5 "Goatsrue is reported to lower blood sugar levels, as well as prevent diabetes mellitus, and can be found sold as a herbal supplement. However, several studies done on its hypoglycemic activity have not been able to prove its abilities to lower blood sugar."
Goat’s rue, galegine, and metformin - Michael H Parker - Feb 2014
How does Goat's Rue or French Lilac work to treat diabetes mellitus? EBM Consult
"While guanidine containing supplements have glucose lowering properties, the toxicity profile outweighs any potential benefits provided and should not generally be used or recommended."
J Clin Invest. 2001 Oct 15; 108(8): 1105–1107.
The blooming of the French lilac
Lee A. Witters
"guanidine itself and certain derivatives are too toxic for the treatment of diabetes mellitus".
Goat's Rue or French lilac (Galega officinalis) contains the active ingredients guanidine and galegine (isoamylene guanidine), which decrease blood sugar and were used in the past to treat diabetes. The plant's hypoglycaemic properties led to the synthesis of metformin, a biguanide compound, because the plant itself was considered too toxic for clinical use. Both guanadine and galegine are toxic, and may cause liver and kidney damage, low blood pressure, ataxia, seizures and lactic acidosis.
The questions to be asked are:
Is Goat's Rue toxic to horses?
Does Goat's Rue help horses with EMS by increasing insulin sensitivity?
Toxicity
The FDA Poisonous Plant Database has 42 listings for Goat's Rue/Gelaga officinalis, mostly relating to the poisoning of sheep.
Veterinary Toxicology: Basic and Clinical Principles - Ramesh Chandra Gupta 2012 p 1087
Galegine decreases blood pressure and paralyses the central nervous system. Poisoning generally affects sheep but cattle have been poisoned. Goat's Rue is bitter and poisoning usually follows the consumption of hay or freshly cut fodder.
Symptoms (hydrothorax) appear 12-24 hours after ingestion, leading to death within hours.
J Ethnopharmacol. 2008 Feb 28;116(1):21-6. Epub 2007 Oct 30
Acute and subchronic oral toxicity of Galega officinalis in rats
Rasekh HR, Nazari P, Kamli-Nejad M, Hosseinzadeh L
"sinusoidal congestion in liver and alveolar hemorrhage was observed"... suggesting that "liver and lung could serve as target organs in oral toxicity of this plant".
Hypoglycaemic/insulin sensitising properties
Goatsrue (Galega officinalis) Seed Biology, Control, and Toxicity
Michelle Oldham MSc Thesis Utah State University 2008
P 5 "Goatsrue is reported to lower blood sugar levels, as well as prevent diabetes mellitus, and can be found sold as a herbal supplement. However, several studies done on its hypoglycemic activity have not been able to prove its abilities to lower blood sugar."
Goat’s rue, galegine, and metformin - Michael H Parker - Feb 2014
How does Goat's Rue or French Lilac work to treat diabetes mellitus? EBM Consult
"While guanidine containing supplements have glucose lowering properties, the toxicity profile outweighs any potential benefits provided and should not generally be used or recommended."
J Clin Invest. 2001 Oct 15; 108(8): 1105–1107.
The blooming of the French lilac
Lee A. Witters
"guanidine itself and certain derivatives are too toxic for the treatment of diabetes mellitus".
Grass
Grasses form the graminae family. Forage is the primary feed of horses, forming ~ 50 - 100% of the horse's diet (DM) as grazed grass, hay, haylage and in some countries, silage.
For information about grass and hay relating to carbohydrate levels and laminitis, see Katy Watts' website:
www.safergrass.org
J Nutr. 2006 Jul;136(7 Suppl):2099S-2102S. (Full paper)
Pasture nonstructural carbohydrates and equine laminitis.
Longland AC, Byrd BM.
Does grass cause laminitis?
The short answer is no - grass doesn't CAUSE laminitis, but it can TRIGGER laminitis. Horses that seem to get laminitis from grass are likely to have an underlying "insulin dysregulation" - EMS/PPID. Grass can contain quite high levels of sugar, leading to raised blood glucose and consequently large amounts of insulin being released. Horses with insulin resistance produce a lot of insulin to deal with the glucose, and the high levels of insulin (hyperinsulinaemia) are thought to be what causes laminitis.
See Talk About Laminitis - Grass & Laminitis (however, be aware that there is currently no valid research that supports the view that fructans in grass increase insulin levels or cause laminitis - see Do fructans cause laminitis?).
How much grass does a horse eat?
Martinson KL, Siciliano PD, Sheaffer CC, McIntosh BJ, Swinker AM, Williams CA
A Review of Equine Grazing Research Methodologies
JEVS published online 14 January 2017
Glunk EC
Effect of Restricted Grazing on Dietary Energy Intake, Dry Matter Intake Rates, and Fecal pH
MSc thesis 2012
Horses with restricted access to pasture ate grass more quickly when they did have access to it.
KER Equinews article by Dr Kathleen Crandell - Revelations About Ponies and Pastures
Unrestricted grazing: the average grass intake of 4 non-working adult ponies over 6 weeks was 3.8% of bodyweight (BW). The ponies gained an average of almost 1kg per day (consuming mixed grass/legume pasture with digestible energy ranging from 2.3 Mcal/kg DM to 2.9 Mcal/kg DM), exceeding their energy requirements.
On average, the ponies ate less higher digestible energy grass (3.4% BW) than lower digestible energy grass (4.2% BW).
A Longland, J Ince, P Harris (2011) Estimation of pasture intake by ponies from liveweight change during six weeks at pasture
J Equine Veterinary Science 31: 275-276
Restricted grazing: ponies allowed 3 hours grazing (and ad-lib low NSC haylage the rest of the time) gained an average of 0.34 kg per day over 6 weeks, and ate an average of 2-2.2% BW in grass and haylage. During week one the ponies ate an average of 0.49% BW grass in 3 hours, by week six they were eating an average of 0.91% BW grass in 3 hours - almost half of their daily feed requirement - and less haylage. Conclusion: limiting turnout is only moderatively effective at reducing grass intake once ponies know the routine.
J. Ince, A. Longland, C. J. Newbold, & P. Harris.(2011) Changes in proportions of dry matter intakes by ponies with access to pasture and haylage for 3 and 20 hours per day respectively for six weeks. J Equine Veterinary Science 31: 283
Use of muzzles: ponies allowed to graze for 3 hours with a muzzle ate an average of 0.14% BW, 83% less than ponies without a muzzle - muzzled ponies did not eat more than 0.5 kg DM compared to unmuzzled ponies who ate around 3.3 kg DM (an average of 0.8% BW).
A Longland, P Harris, C Barfoot, (2011) The effect of wearing a grazing muzzle vs not wearing a grazing muzzle on pasture dry matter intake by ponies. J Equine Veterinary Science 31: 282-283
For information about grass and hay relating to carbohydrate levels and laminitis, see Katy Watts' website:
www.safergrass.org
J Nutr. 2006 Jul;136(7 Suppl):2099S-2102S. (Full paper)
Pasture nonstructural carbohydrates and equine laminitis.
Longland AC, Byrd BM.
Does grass cause laminitis?
The short answer is no - grass doesn't CAUSE laminitis, but it can TRIGGER laminitis. Horses that seem to get laminitis from grass are likely to have an underlying "insulin dysregulation" - EMS/PPID. Grass can contain quite high levels of sugar, leading to raised blood glucose and consequently large amounts of insulin being released. Horses with insulin resistance produce a lot of insulin to deal with the glucose, and the high levels of insulin (hyperinsulinaemia) are thought to be what causes laminitis.
See Talk About Laminitis - Grass & Laminitis (however, be aware that there is currently no valid research that supports the view that fructans in grass increase insulin levels or cause laminitis - see Do fructans cause laminitis?).
How much grass does a horse eat?
Martinson KL, Siciliano PD, Sheaffer CC, McIntosh BJ, Swinker AM, Williams CA
A Review of Equine Grazing Research Methodologies
JEVS published online 14 January 2017
Glunk EC
Effect of Restricted Grazing on Dietary Energy Intake, Dry Matter Intake Rates, and Fecal pH
MSc thesis 2012
Horses with restricted access to pasture ate grass more quickly when they did have access to it.
KER Equinews article by Dr Kathleen Crandell - Revelations About Ponies and Pastures
Unrestricted grazing: the average grass intake of 4 non-working adult ponies over 6 weeks was 3.8% of bodyweight (BW). The ponies gained an average of almost 1kg per day (consuming mixed grass/legume pasture with digestible energy ranging from 2.3 Mcal/kg DM to 2.9 Mcal/kg DM), exceeding their energy requirements.
On average, the ponies ate less higher digestible energy grass (3.4% BW) than lower digestible energy grass (4.2% BW).
A Longland, J Ince, P Harris (2011) Estimation of pasture intake by ponies from liveweight change during six weeks at pasture
J Equine Veterinary Science 31: 275-276
Restricted grazing: ponies allowed 3 hours grazing (and ad-lib low NSC haylage the rest of the time) gained an average of 0.34 kg per day over 6 weeks, and ate an average of 2-2.2% BW in grass and haylage. During week one the ponies ate an average of 0.49% BW grass in 3 hours, by week six they were eating an average of 0.91% BW grass in 3 hours - almost half of their daily feed requirement - and less haylage. Conclusion: limiting turnout is only moderatively effective at reducing grass intake once ponies know the routine.
J. Ince, A. Longland, C. J. Newbold, & P. Harris.(2011) Changes in proportions of dry matter intakes by ponies with access to pasture and haylage for 3 and 20 hours per day respectively for six weeks. J Equine Veterinary Science 31: 283
Use of muzzles: ponies allowed to graze for 3 hours with a muzzle ate an average of 0.14% BW, 83% less than ponies without a muzzle - muzzled ponies did not eat more than 0.5 kg DM compared to unmuzzled ponies who ate around 3.3 kg DM (an average of 0.8% BW).
A Longland, P Harris, C Barfoot, (2011) The effect of wearing a grazing muzzle vs not wearing a grazing muzzle on pasture dry matter intake by ponies. J Equine Veterinary Science 31: 282-283
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How much sugar/NSC is in grass?
The sugars and non structural carbohydrates found in grass are categorized as: 1. ESC (ethanol soluble carbohydrates) - also known as simple sugars, ESC is the total of the monosaccharides glucose and fructose and the disaccharide sucrose. A sucrose molecule consists of 1 glucose and 1 fructose molecule. ESC may also contain short-chain fructans. Glucose, fructose and sucrose are digested and absorbed in the small intestine and affect insulin (and therefore can trigger endocrinopathic laminitis in horses with EMS and PPID). 2. WSC (water soluble carbohyrates) - WSC is the total of ESC plus long and short chain fructans. Fructans are not digested in the small intestine (although there may be a small amount of pre-cecal fermentation of fructans), they pass to the cecum and large intestine where they are fermented by micro-organisms to volatile fatty acids (VFAs). 3. NSC (non structural carbohyrates - NSC is the total of WSC plus starch. Starch is digested to and absorbed as glucose in the small intestine, and in the same way as ESC affects insulin and can trigger endocrinopathic laminitis. |
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Kagan IA, Lawrence LM, Seman DH, Prince KJ, Fowler AL, Smith SR
Effects of sampling time, cultivar, and methodology on water- and ethanol-soluble carbohydrate profiles of three cool-season grasses in central Kentucky
JEVS published online Nov 2017
Effects of sampling time, cultivar, and methodology on water- and ethanol-soluble carbohydrate profiles of three cool-season grasses in central Kentucky
JEVS published online Nov 2017
Is lush/rich/short/long/dead grass high in sugar?
Green "lush" grass may not have significantly different NSC levels to grass that is short and brown. "Lush" does not imply high sugar or starch - see Lushness is not a factor in the water soluble carbohydrate or starch concentration of grass - Kathryn Watts www.safergrass.org
How does grass affect fecal pH?
Cassie Wycoff MSc thesis 2013
Effect of Time of Day During Grazing on Hindgut Fermentation Parameters in Cool Season Grass Pasture-fed Horses
Glunk EC MSc thesis 2012
Effect of Restricted Grazing on Dietary Energy Intake, Dry Matter Intake Rates, and Fecal pH
How does grass affect VFA production?
Cassie Wycoff MSc thesis 2013
Effect of Time of Day During Grazing on Hindgut Fermentation Parameters in Cool Season Grass Pasture-fed Horses
How does grass management affect NSC levels?
Siciliano PD, Gill JC, Bowman MA
Effect of Sward Height on Pasture Nonstructural Carbohydrate Concentrations and Blood Glucose/Insulin Profiles in Grazing Horses
JEVS October 2017 vol 57, Pages 29–34
6 geldings grazed either 15 cm or 30-40 cm high tall fescue (Lolium arundinaceum) paddocks for 10 hours per day (from 8 am until 6 pm) for 7 days, then crossed over. No feed was given to the horses from 6 pm to 8 am.
The 15 cm paddocks were mowed to 15 cm 32 days and 11 days before the study started, and 1 day before the horses were introduced to the paddocks.
The 30-40 cm paddocks were mowed to 15 cm 32 days before the study started.
On day 7 of each grazing period, blood was collected and tested for insulin and glucose, and pasture sampled and tested for WSC, ESC and starch, before turnout and at 2, 4, 6 and 8 hours after turn out
Mean WSC and ESC % were lower in the 15 cm grass than the 30-40 cm grass.
Pregrazing glucose and insulin were not affected by treatment.
Postgrazing plasma glucose was not different between horses grazing different height grass.
Postgrazing serum insulin was greater in horses horses grazing 30-40 cm grass than in horses grazing 15 cm grass.
"In conclusion, decreasing the sward height by mowing pasture decreased NSC, WSC, and ESC concentrations and subsequently decreased the postprandial insulin response of horses grazing the pasture. These findings may be important in developing strategies aimed at preventing insulin resistance in grazing horses."
Mowing (topping) decreased fructan and glucose levels but only transiently - fructan levels halved 30 hours after mowing but returned to normal 60 hours after mowing:
Howieson MJ, Christians NE
Carbohydrate Metabolism and Efficiency of Photosystem II in Mown Creeping Bentgrass (Agrostis stoloniferaL.)
HortScience April 2008 vol. 43 no. 2 525-531
WSC levels decreased to around 50% of their original concentrations 4 days after mowing, and returned to their original concentrations by day 24 - sucrose and fructan levels declined more than mono-saccharide (reducing sugar) levels:
Volenec JJ
Nonstructural Carbohydrates in Stem Base Components of Tall Fescue During Regrowth
Crop Sci. 1986. 26:122–127
Research giving insulin concentrations after grazing grass
Williams CA, Kenny LB, Burk AO.
Effects of grazing system, season, and forage carbohydrates on glucose and insulin dynamics of the grazing horse.
J Anim Sci. 2019 May 30;97(6):2541-2554. doi: 10.1093/jas/skz103. PMID: 30911753; PMCID: PMC6541809.
Keywords: carbohydrate, continuous grazing, equine, glucose, insulin, rotational grazing
McIntosh Bridgett PhD dissertation December 2006
Circadian and Seasonal Variation in Pasture Nonstructural Carbohydrates and the Physiological Response of Grazing Horses
Growth hormone
Growth Hormone (Somatotropin) - Colorado State University (2006)
Growth hormone injections increased serum insulin concentrations and caused variable hyperinsulinaemia:
Noble GK, Sillence MN
Diurnal rhythm and effects of feeding, exercise and recombinant equine growth hormone on serum insulin concentrations in the horse
Equine Veterinary Journal online Jan 2013
Growth hormone injections increased serum insulin concentrations and caused variable hyperinsulinaemia:
Noble GK, Sillence MN
Diurnal rhythm and effects of feeding, exercise and recombinant equine growth hormone on serum insulin concentrations in the horse
Equine Veterinary Journal online Jan 2013