Insulin renal metabolism

In renal insufficiency the renal metabolism of insulin is impaired and generation of glucose reduced (178). 

Insulin resistance occurs when the normal response to a given amount of insulin is reduced. Resistance of liver to the effects of insulin results in inadequate suppression of hepatic glucose production insulin resistance of skeletal muscle reduces the amount of glucose taken out of the circulation into skeletal muscle for storage and insulin resistance of adipose tissue results in impaired suppression of lipolysis and increased levels of free fatty acids. Therefore, insulin resistance is associated with a cluster of metabolic abnormalities including elevated blood glucose levels, abnormal blood lipid profile (dyslipidemia), hypertension, and increased expression of inflammatory markers (inflammation). Insulin resistance and this cluster of metabolic abnormalities is strongly associated with obesity, predominantly abdominal (visceral) obesity, and physical inactivity and increased risk for type 2 diabetes, cardiovascular and renal disease, as well as some forms of cancer. In addition to obesity, other situations in which insulin resistance occurs includes... 

Disorders of lipoprotein metabolism involve perturbations which cause elevation of triglycerides and/or cholesterol, reduction of HDL-C, or alteration of properties of lipoproteins, such as their size or composition. These perturbations can be genetic (primary) or occur as a result of other diseases, conditions, or drugs (secondary). Some of the most important secondary disorders include hypothyroidism, diabetes mellitus, renal disease, and alcohol use. Hypothyroidism causes elevated LDL-C levels due primarily to downregulation of the LDL receptor. Insulin-resistance and type 2 diabetes mellitus result in impaired capacity to catabolize chylomicrons and VLDL, as well as excess hepatic triglyceride and VLDL production. Chronic kidney disease, including but not limited to end-stage... 

As to be expected from a peptide that has been highly conserved during evolution, NPY has many effects, e.g. in the central and peripheral nervous system, in the cardiovascular, metabolic and reproductive system. Central effects include a potent stimulation of food intake and appetite control [2], anxiolytic effects, anti-seizure activity and various forms of neuroendocrine modulation. In the central and peripheral nervous system NPY receptors (mostly Y2 subtype) mediate prejunctional inhibition of neurotransmitter release. In the periphery NPY is a potent direct vasoconstrictor, and it potentiates vasoconstriction by other agents (mostly via Yi receptors) despite reductions of renal blood flow, NPY enhances diuresis and natriuresis. NPY can inhibit pancreatic insulin release and inhibit lipolysis in adipocytes. It also can regulate gut motility and gastrointestinal and renal epithelial secretion. 

Patients predicted to follow a severe course require treatment of any cardiovascular, respiratory, renal, and metabolic complications. Aggressive fluid resuscitation is essential to correct intravascular volume depletion and maintain blood pressure. IV colloids may be required because fluid losses are rich in protein. Drotrecogin alfa may benefit patients with pancreatitis and systemic inflammatory response syndrome. IV potassium, calcium, and magnesium are used to correct deficiency states. Insulin is used to treat hyperglycemia. Patients with necrotizing pancreatitis may require antibiotics and surgical intervention. 

Renal disease or renal dysfunction (eg, as suggested by serum creatinine levels greater than or equal to 1.5 mg/dL [males], greater than or equal to 1.4 mg/dL [females], or abnormal Ccr) that may also result from conditions such as cardiovascular collapse (shock), acute myocardial infarction (Ml), and septicemia CHF requiring pharmacologic treatment hypersensitivity to metformin acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. Treat diabetic ketoacidosis with insulin. 

II.f.2.2. Sulphonylureas. These drugs stimulate pancreatic /3-cell insulin secretion, reduce serum glucagon levels, potentiate insulin action on target tissues, and improve /3-cell function. The sulphonylureas differ in their potency, extent of hepatic metabolism, hypoglycaemic activity of their metabolites, renal excretion, peak and duration of action, side effects and costs. 

Managing the Complications of Diabetes. Diabetes is more than just a disorder of elevated glucose it is a systemic disease that affects many organ systems. In addition to the metabolic problems there are numerous neurological, circulatory, and renal complications, even when the blood glucose level is properly controlled. The main reason is the unnatural administration of insulin by injection, instead of the constant secretion by the pancreas in response to changing blood glucose levels. Diabetics have a predisposition of atherosclerosis, with an increased risk for heart attacks and stroke. 

DeFronzo RA. The effect of insulin on renal sodium metabolism. A review with clinical implications. Diabetologia 1981 21(3) 165-71. 

Depression and Metabolic Syndrome. Abnormal serum albumin levels and lipid profiles have both been observed in patients with major depression, as well as cardiovascular disease, diabetes mellitus, and end-stage renal disease. Depressive symptoms are very common in patients with these chronic illnesses. Recent clinical data have shown that cardiovascular disease, diabetes mellitus, end-stage renal disease, and obesity are all related to metabolic syndromes [68-74], and especially insulin resistance [75, 76]. However, the data examining major depression without physical illness and insulin resistance are still scarce. In the future, the biological relationship between depression and physical illness needs to be more fully explored. 

Sulphonylureas stimulate the release of insulin and undergo extensive first-pass hepatic metabolism by the cytochrome P450 system (and therefore adverse drug interactions with inducers and inhibitors of cytochrome P450). They are highly protein-bound. Chlorpropramide is the only sulphonylurea with significant renal excretion. 

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