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hyperglycemia caused by tissue insulin resistance and inhibition of anaer-obic glycolysis
فرط سكر الدم بسبب مقاومة الأنسجة للانسولين وتثبيط انحلال السكر اللاهوائي.
it provides metabolic support to the myocardium by increasing anaerobic glycolysis, low-ering free fatty acid levels, preserving intracellular glycogen stores, and stabiliz-ing membrane function.
يُقدّم هذا المزيج الدعم الاستقلابي للعضلة القلبية عن طريق زيادة التحلّل اللاهوائي للسكر، وخفض مستوى الحموض الدسمة الحرة، وحفظ مخازن الغليكوجين داخل الخلايا، والمحافظة على استقرار وظائف الغشاء الخلوي.
metabolic actions of insulin glucose homeostasis serum glucose level is maintained by the balance between glucose production and glucose disposal that are regulated by glucagon and insulin. insulin inhibits glucose production by suppressing glycogenolysis47,48 and gluconeogenesis.49-52 glycogen is a multi-branched polysaccharide of glucose and is stored as an energy source in the liver and skeletal muscle. glycogenolysis is referring to breaking down glycogen to produce glucose-6-phosphate (g6p). g6p is converted to glucose by a glucose-6-phosphatase, and then glucose is released into the bloodstream.53 furthermore, gluconeogenesis is a metabolic pathway of generating glucose from non-carbohydrate carbon substrates.49-52 insulin inhibits the expression of the enzymes such as glucose-6 phosphatase and phosphoenolpyruvate carboxykinase that regulate the rate-limiting steps of gluconeogenesis.54,55 akt inhibits foxo by phosphorylation, which regulates the expression of gluconeogenic enzymes.56-58 insulin also reduces serum glucose levels by stimulating glucose utilization. thus, insulin reduces serum glucose levels by enhancing glucose uptake and glucose utilization by stimulation of glycolysis and glycogen synthesis, and inhibiting hepatic glucose production by suppression of glycogenolysis and gluconeogenesis.51,59-63 lipid metabolism insulin is the major anabolic hormone, which means store energy sources. insulin clears lipids, such as ffa and chylomicrons from circulation and stores it in adipocytes. circulating triglyceride is hydrolyzed by lipoprotein lipase (lpl), which is presented on the surface of capillaries in muscle and fat. insulin stimulates the activity of lpl in the adipose tissue while inhibits lpl in the skeletal muscle.64,65 this tissue-specific regulation of lpl by insulin contributes to directing from fat utilization by skeletal muscle to fat storage by adipose tissue. insulin increases triglyceride contents in fat cells by stimulating the re-esterification of ffa to glycerol-3-phosphate for synthesizing triglyceride and by increasing de novo lipogenesis (dnl) through promoting the expression of fatty acid synthase.66-70 insulin- stimulated lipogenesis is also mediated by the akt/torc1 pathway, increasing the sterol receptor element binding protein-1c.71-74 importantly, torc1 seems to be the molecular link between glucose and lipid metabolism for dnl. furthermore, insulin inhibits lipolysis by inhibiting hormone-sensitive lipase activity through the activation of phosphatase and the inhibition of phosphodiesterase reducing cyclic amp levels in adipocyte.75-78 other nutrient metabolism insulin stimulates amino acid transport into the liver and skeletal muscle, which leads to increased protein synthesis,79 and inhibits proteolysis.80 also, insulin maintains amino acid levels for protein synthesis by inhibiting gluconeogenesis, which generates glucose from amino acids.81 incomplete oxidation of long-chain fatty acids produces ketone bodies and ketoacidosis, which occurs when the liver is supplied excess amount of fatty acids in hypoinsulinemic conditions, including prolonged fasting or uncontrolled dm. insulin lowers circulating ketone body by inhibiting lipolysis in the adipose tissue, which lowers the availability of fatty acids.82 furthermore, insulin facilitates ketone body utilization in skeletal muscle, heart, and brain