Diabetes is considered a disease related to carbohydrates, but in recent years the lipid changes associated with this condition have been described, which generate greater atherosclerosis and could overcome, in damage, the cellular effects of glucose.
Although small vessel disease is related to hyperglycemia, it is difficult to attribute that of large vessels to this phenomenon and glycemic control does not seem to improve cardiovascular disease. Treatments aimed at reducing cholesterol, especially statins, have a significant effect on the rates of cardiovascular events in patients with diabetes.
It has been proven that during the night, in a fasting state, an insulin deficiency occurs that increases blood glucose and triglyceride levels. The latter are stored in different lipoprotein particles that alternate in cascades from chylomicrons to very low, intermediate, low (LDL) and high density (HDL) lipoproteins.
Fasting and postprandial hypertriglyceridemia were associated with cardiovascular events and death; Starvation and bariatric surgery significantly affect plasma lipids and the role of bile acids in cholesterol homeostasis is important.
Insulin action and effect of diacylglycerol
Insulin secretion depends on glucose; this hormone prevents postprandial hyperglycemia and also plays a fasting role (when blood glucose is low); It also prevents the increase of free fatty acids, which stimulate insulin secretion by the beta cells of the pancreas, favor oxygen consumption and increase the rate of extracellular acidification.
Insulin can store excessive calories in adipose tissue if nutrition is excessive, but subsequently fatty acids accumulate in the liver and muscle, and favor insulin resistance (in addition to apoptosis of beta cells). This phenomenon hinders the metabolism of fatty acids and excessive plasma levels induce hyperglycemia, which in turn inhibits beta-oxidation and fatty acids tend to form triglycerides.
Diacylglycerol is a precursor to the synthesis of triglycerides metabolized by specific kinases; When their concentration is high and the activity of these kinases is low, the risk of insulin resistance and type 2 diabetes is higher. Excess nutrients in type 2 diabetes or obesity generates higher circulating levels of diacylglycerol and increased activity of protein kinase C and, on the other hand, reduces the activity of the kinase activated by adenosine monophosphate. Metformin stimulates the latter enzyme, which is important in the metabolism of energy and lipids, and thus inhibits gluconeogenesis.
What medical importance does this have?
Several years ago it was observed that in the transition between normoglycemia, prediabetes and diabetes, the profile of free fatty acids is increasingly anomalous and that the use of enzyme inhibitors synthesized by diacylglycerol from free fatty acids would be useful for improving insulin resistance in adipose tissue and systemic glucose metabolism, with reduced body weight.
The absorption of cholesterol is highly regulated (by transporters such as NPC1L1) and fatty acids stimulate the synthesis of apo-B100, which is modified to apo-B48 (very atherogenic particle that transports triglycerides and cholesterol to the liver) in the intestine.
Diabetes affects the metabolism of triglyceride-rich lipoproteins and makes them more atherogenic. Since in the hyperglycemia states the production of free radicals increases, there is greater oxidation of LDL. In individuals with diabetes the antioxidant and beneficial effect of HDL would be less.
Finally, it can be concluded that there is an interconnection between blood glucose and dyslipidemia alterations, and both disorders are enhanced, leading to the development of cardiovascular diseases.
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