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The cat is monitored frequently during the first few months of treatment; The cat eats a diet low in carbohydrates and high in protein. Cats may present with type 2 (insulin-resistant) diabetes, at least at first, but hyperglycemia and amyloidosis, left untreated, will damage the pancreas over time and progress to insulin-dependent diabetes.
Rarely some cats will redevelop hyperthyroidism up to 6 years after treatment, this is likely due to new foci caused by new mutations in the tissue than any failure of treatment. [ 2 ] The average age of death for a cat that has received radioactive iodine treatment for hyperthyroidism is 15 years.
The causes of the aging-related insulin resistance seen in obesity and in type 2 diabetes are uncertain. Effects of intracellular lipid metabolism and ATP production in liver and muscle cells may contribute to insulin resistance. [62]
The causes of feline hyperesthesia syndrome are highly disputed, largely due to the unknown pathophysiology of the syndrome and the variation in responses to different treatment methods. [ 1 ] [ 3 ] [ 4 ] [ 8 ] There are three main theories on the cause of the syndrome, as outlined below:
This leads to excessive urination (more specifically an osmotic diuresis), which, in turn, leads to volume depletion and hemoconcentration that causes a further increase in blood glucose level. Ketosis is absent because the presence of some insulin inhibits hormone-sensitive lipase-mediated fat tissue breakdown. [citation needed]
More than 38 million Americans have diabetes, and between 90% and 95% of them have type 2 diabetes. While most are adults over the age of 45, an increasing number of children and teens are also ...
Diabetes mellitus causes a disruption in the body's ability to transfer glucose from food into energy. [clarification needed] Polyphagia in type 2 diabetes is usually not as apparent as the polyphagia in type 1 diabetes. In type 1 diabetes, it probably results from cellular starvation and the depletion of cellular stores of carbohydrates, fats ...
Thiazolidinedione ligand dependent transactivation is responsible for the majority of anti-diabetic effects. The activated PPAR/RXR heterodimer binds to peroxisome proliferator hormone response elements upstream of target genes in complex with a number of coactivators such as nuclear receptor coactivator 1 and CREB binding protein, this causes upregulation of genes (for a full list see PPARγ):
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