Shubham Sharma*

M.V.Sc Scholar, Veterinary Pathology, Ranchi Veterinary College, Kanke, Jharkhand, India

*Corresponding Author: Shubham Sharma, M. V. Sc Scholar, Veterinary Pathology, Ranchi Veterinary College, Kanke, Jharkhand, India.

Received: May 21, 2024; Published: June 28, 2024

Abstract

Glucose homeostasis refers to the processes involved in the production, storage and release of glucose from Storage. Glucose is derived by the ingestion, digestion and absorption of carbohydrates, and blood glucose is maintained within tight limits by several different mechanisms. In addition, in processes particularly important in cats, gluconeogenesis and glycogenolysis allow glucose to be made within the body from other substrates. Reference ranges vary according to the laboratory and testing method but 3.0-6.5 mmol/l in dogs and 3.1-7.2 mmol/l in Cats are generally acceptable glucose concentrations that are unlikely to cause clinical signs in most animals. Hypoglycaemia is a life-threatening condition generally defined by a blood glucose lower than 3 mmol/l. Clinical Signs are not always apparent at a blood glucose level of 3 mmol/l, although a rapid fall in blood glucose, for example following an accidental insulin over-dose in a diabetic patient, may lead to clinical signs at a higher blood glucose concentration if there has not been sufficient time for counter-regulatory mechanisms to take effect. Hyperglycaemia is most commonly encountered in stressed animals and in patients with diabetes mellitus. Canine diabetes is usually the result of insulin deficiency and a classification scheme has been described. Diabetic ketosis is another complication due to hyperglycaemia , Fatty acid mobilization and ketone body formation resulting in ketosis. NKHS is another syndrome but with absence of ketone in it.

 Keywords: Homeostasis; Diabetes Mellitus; Ketosis; NKHS

References

1. Alt N., et al. “Day-to-day variability of blood glucose concentration curves generated at home in cats with diabetes mellitus”. Journal of the American Veterinary Medical Association 230 (2007): 1011-1017.
2. Boari A., et al. “Hypoglycemia in a dog with a leiomyoma of the gastric wall producing an insulin-like growth factor II-like peptide”. European Journal of Endocrinology 132 (1995): 744-750.
3. Bruskiewicz KA., et al. “Diabetic ketosis and ketoacidosis in cats: 42 cases (1980-1995)”. Journal of the American Veterinary Medical Association 211 (1997): 188-192.
4. Davison LJ., et al. “Study of 253 dogs in the United Kingdom with diabetes mellitus”. Veterinary Record 156 (2005): 467-471.
5. Davison LJ., et al. “Evaluation of a continuous glucose monitoring system in diabetic dogs”. Journal of Small Animal Practice 44 (2003): 435-442.
6. Davison LJ., et al. “Anti-insulin antibodies in diabetic dogs before and after treatment with different insulin preparations”. Journal of Veterinary Internal Medicine 22 (2008): 1317-1325.
7. Dunayer EK. “Hypoglycemia following canine ingestion of xylitol containing gum”. Veterinary and Human Toxicology 46 (2004): 87-88.
8. Hoenig M. “The cat as a model for human obesity and diabetes”. Journal of Diabetes Science and Technology 6 (2012): 525-533.
9. Hoenig M., et al. “Beta cell and insulin antibodies in treated and untreated diabetic cats”. Veterinary Immunology and Immunopathology 77 (2000): 93-102.
10. Hume DZ., et al. “Outcome of dogs with diabetic ketoacidosis: 127 dogs (1993-2003)”. Journal of Veterinary Internal Medicine 20 (2006): 547-555.
11. Johnson CA. “Glucose homeostasis during canine pregnancy: Insulin resistance, ketosis, and hypoglycemia”. Theriogenology 70 (2008): 1418-1423.
12. Klein SC and Peterson ME. “Canine hypoadrenocorticism: part I”. Canadian Veterinary Journal 51 (2010): 63-69.
13. Macintire DK. “Emergency therapy of diabetic crises: insulin overdose, diabetic ketoacidosis, and hyperosmolar coma”. Veterinary Clinics of North America: Small Animal Practice 25 (1995): 639-650
14. Mansfield C. “Acute pancreatitis in dogs: advances in understanding, diagnostics, and treatment”. Topics in Companion Animal Medicine 27 (2012): 123-132.
15. Mattheeuws D., et al. “Diabetes mellitus in dogs: relationship of obesity to glucose tolerance and insulin response”. American Journal of Veterinary Research 45 (1984): 98-103.
16. McCann TM., et al. “Feline diabetes mellitus in the UK: the prevalence within an insured cat population and a questionnaire-based putative risk factor analysis”. Journal of Feline Medicine and Surgery 9 (2007): 289-299.
17. Niessen SJ. “Feline acromegaly: an essential differential diagnosis for the difficult diabetic”. Journal of Feline Medicine and Surgery 12 (2010): 15-23.
18. Paul AE., et al. “Effect of hematocrit on accuracy of two point-of-care glucometers for use in dogs”. American Journal of Veterinary Research 72 (2011): 1204-1208.
19. Rand JS., et al. “Canine and feline diabetes mellitus: nature or nurture?” Journal of Nutrition 134 (2004): 2072S-2080S.
20. Rand JS., et al. “Acute stress hyperglycemia in cats is associated with struggling and increased concentrations of lactate and norepinephrine”. Journal of Veterinary Internal Medicine 16 (2002): 123-132.
21. Sieber-Ruckstuhl NS., et al. “Remission of diabetes mellitus in cats with diabetic ketoacidosis”. Journal of Veterinary Internal Medicine 22 (2008): 1326-1332.
22. Willard MD., et al. “Severe hypophosphatemia associated with diabetes mellitus in six dogs and one cat”. Journal of the American Veterinary Medical Association 190 (1987): 1007-1010.
23. Xenoulis PG and Steiner JM. “Current concepts in feline pancreatitis”. Topics in Companion Animal Medicine 23 (2008): 185-192.

Citation

Citation: Shubham Sharma. “Pathological Evaluation of Hypoglycemia and Hyperglycemia in Canines and Felines". Acta Scientific Veterinary Sciences 6.7 (2024): 45-54.

Copyright

Copyright: © 2024 Shubham Sharma. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.