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Pathophysiology of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Insulin is an anabolic hormone, normally present in individuals that consume healthy diets. It is a signaling factor that stimulates storage of excess nutrients, including glycogen and triglycerides, in the form of adipose fat. Insulin mostly affects the liver, adipose tissue, and striated muscles. Its synthesis and release is stimulated by glucose, but potentiated by amino acids. In the liver, insulin stimulates glycogenesis, fatty acid synthesis, glycolysis, and the pentose phosphate pathway. In adipose tissue, insulin stimulates uptake of glucose and fatty acids, and triglyceride synthesis. This is also known as energy storage. In skeletal muscles, insulin stimulates glucose uptake, glycogenesis, and synthesis of proteins. Insulin does not influence metabolism of glucose in the brain or red blood cells.
Alcohol
Published in T.M. Craft, P.M. Upton, Key Topics In Anaesthesia, 2021
Alcohol has a direct diuretic effect while the blood level is rising, increasing free water clearance. There maybe a fall in serum potassium and magnesium. Gluconeogenesis is inhibited and glycogenesis enhanced. This may result in hypoglycaemia up to 30 hours after alcohol consumption in the fasted patient.
Features of Lipid Metabolism in Diabetes Mellitus and Ischemic Heart Disease
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
The transportation and metabolic effects of insulin are a result of binding of the hormone to the membrane receptors. In hyperinsulinemia of any etiology, the number of receptors in the adipose tissue and muscles lowers appreciably, while with normalization of the insulin level the number of receptors is restored. The clinical picture of obesity combines with hyperglycemia, hyperinsulinemia, a reduction of glycogen synthesis in the liver, and enhancement of the glycogenesis process. It is the reciprocal nature of the reaction between the growth in the activity of the enzymes of glycogenesis and the inhibition of the activity of the glycolysis enzymes that disturbs lipid metabolism. Already in the early stages of obesity, hyperlipidemia, hypercholesterolemia, hypertriglyceridemia, and a growth in the FFA level are noted in the patients.
Inflammation, oxidative stress and altered heat shock response in type 2 diabetes: the basis for new pharmacological and non-pharmacological interventions
Published in Archives of Physiology and Biochemistry, 2022
Gabriela Elisa Hirsch, Thiago Gomes Heck
In addition to the participation of inflammation in the pathogenesis of diabetes, oxidative stress has also demonstrated an important role in the disease and its complications. Many studies with experimental models of diabetes have reported that oxidative stress induced by hyperglycaemia plays an important role in hepatic dysfunction and renal damage and that the administration of antioxidant agents has the ability to recover the function of these organs (Abo-Salem et al.2009, Gomes et al.2015, Iskender et al.2017). The liver plays an important role in blood glucose homeostasis. It provides the balance between storage and uptake of glucose via glycogenesis. The imbalance in glucose regulation due to diabetes mellitus results in chronic tissue damage and organ failure (Levinthal 1999).
Assessment of antidiabetic potential of Musa acuminata peel extract and its fractions in experimental animals and characterisation of its bioactive compounds by HPTLC
Published in Archives of Physiology and Biochemistry, 2022
Navghare Vijay, Dhawale Shashikant, Phanse Mohini
The possible mechanism of action of antidiabetic effects of extract and fractions of Musa acuminata peels might include its insulinogenic effects. As insulin is the main regulator of glycogenesis in muscle and liver; insulin deficiency in DM leads to decrease in the hepatic and skeletal muscle glycogen content (William and Goldberg 1967). Estimation of liver glycogen is considered as the one of the marker for assessing the antihyperglycemic effect of any drug (Ahmed et al.2012). In the current findings, the liver glycogen content in diabetic animals treated with EMA-400 was significantly increased. This effect might be due to improvement in glycogenesis and/or reduction in glycogenolysis in the liver (Ramkumar et al.2011). Increased glycogen content may be due to increased insulin response which enhances the formation of the active form of glycogen synthase from inactive form and thereby promotes the formation of glycogen from blood glucose. Dietary fibres prepared from unripe banana, reduces fasting glucose level and increase glycogen content (The Wealth of India 2003).
In silico and in vivo analysis to identify the antidiabetic activity of beta sitosterol in adipose tissue of high fat diet and sucrose induced type-2 diabetic experimental rats
Published in Toxicology Mechanisms and Methods, 2019
R. Ponnulakshmi, B. Shyamaladevi, P. Vijayalakshmi, J. Selvaraj
An impaired glucose uptake and oxidation in adipose tissue were also observed in the high-fat diet and sucrose-fed diabetic rats as a result of reduced levels of GLUT4 in the plasma membrane which is responsible for glucose transport. β-sitosterol treatment restored it to the normal range as a result of increase in GLUT 4 level in both cytosol and plasma membrane of adipose tissue of diabetic rats. Chai et al.(2011) reported β-sitosterol-induced glucose uptake in rat preadipocytes and suggested that β-sitosterol has insulin-like activity, besides being an insulin secretagogue which supports our present study. A significant decrease in glycogen concentration was also observed in high fat and sucrose-fed rats, which may be attributed to impairment in glycogenesis due to insulin resistance (Cross et al. 1995; Sathish and Balasubramanian 2014). β-sitosterol treated diabetic rats showed a significant increase in glycogen content. In this regard, Ramu et al. (2016) also reported increased levels of hepatic glycogen and glycogen synthase and the corresponding decrease of glycogen phosphorylase activity in β-sitosterol treated alloxan-induced diabetic rats. The enhanced glucose uptake, oxidation and glycogen level observed in the β-sitosterol administered diabetic rats may be attributed by the improved activity of insulin signaling molecules and increased GLUT4 level in adipose tissue.