The endocrine pancreas has various types of cells including:
- Α cells responsible for the production of the hormone glucagon, which stimulates the production of glucose by the hepatic cells (liver), therefore has a hyperglycemic effect (increases blood sugar).
- Β cells that produce insulin, which has a hypoglycemic effect (lowers blood sugar), because it determines the uptake of blood glucose (found in the blood) by the cells and inhibits its production by the liver.
The synergistic action of insulin and glucagon therefore makes it possible to regulate blood sugar, keeping it at physiological values ranging from 70 to 110 mg / dl. In a nutshell, when there is a need for glucose (primary energy source) by the cells, glucagon causes this to be produced by the liver and put into circulation (increased blood sugar) and then picked up by the cells that use it. thanks to insulin (which causes hypoglycemia).
(the glycerol incorporated in the triglyceride molecule) and proteins (which determine the weight loss of the animal). Furthermore, there is polyphagia (increased appetite), because insulin is also responsible for the "activation of the" center of satiety ", which, in the absence of this" hormone, is not activated and therefore induces a constant appetite which causes a further increase in blood sugar.
At the renal level, generally, glucose passes the renal filter and is then reabsorbed, again by the kidney, by the so-called proximal convoluted tubule. If the glucose concentrations in the blood are excessive (marked hyperglycemia), as occurs in diabetes, the kidney is no longer able to reabsorb all the glucose, which therefore passes partly in the urine (glycosuria). Being an osmotically active molecule (it attracts water), glucose prevents the reabsorption of water by the kidney, resulting in polyuria (increased urine output).
In turn, the excessive loss of water with urine causes hypotension (low pressure) which, in addition to having a negative effect on various organs, including the kidney, stimulates the animal to take in a lot of water (polydipsia) .
(clouding of the lens with loss of vision) is probably the most frequent complication, which occurs in dogs with diabetes mellitus. The alterations of the lens (part of the eye) occur because the constant hyperglycemia determines an accumulation of carbohydrates in the lenses (crystallines) which indirectly cause a break in the fibers of the lenses themselves.
Diabetic ketoacidosis (DKA) is perhaps the most serious complication that can be found, in the vast majority of cases, in animals in which it was unknown that they were suffering from diabetes mellitus and therefore not undergoing therapy. Prolonged insulin deficiency determines, over time, a greater use of lipids to produce energy at the expense of carbohydrates. This leads to the production, then to the accumulation, of circulating ketone bodies which cause metabolic acidosis (the animal suffers from halitosis: breath that tastes like acetone). Then when the ketones reach such concentrations that they are no longer reabsorbed by the kidney, they are poured into the urine (ketonuria), increasing diuresis and the excretion of electrolytes (sodium, potassium, magnesium). The metabolic alterations caused by DKA can seriously endanger the life of the animal.
Diabetic neuropathy is also a common consequence in cats suffering from diabetes mellitus. Although the cause is not yet fully understood, this complication arises with motor deficits (cats, while walking, support their hocks), weakness, incoordination and lack of reflexes.
Finally, as a consequence of all those metabolic alterations caused by untreated diabetes mellitus, we can have complications such as pancreatitis (inflammation of the pancreas), hepatic lipidosis (accumulation of lipids in the liver), retinopathy (disease of the retina), bacterial infections and glomerulonephropathy. (pathology of the kidney).
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