Diabetes fatty acids levels

ATP sensitive K channels. They lower down the blood sugar level in type 11 diabetics and non-diabetic individuals. They also decrease the elevated plasma free fatty acid levels. They also sensitize the target tissues to action of insulin by increasing the number of insulin receptors. 

The most prevalent form of diabetes, which accounts for 85-95% of all cases, is type 2 diabetes, defined by reduced insulin production and insulin resistance. Insulin resistance occurs when increasing quantities of insulin are required to regulate the transport of plasma glucose to body tissues. It is often accompanied by obesity, which elevates the free fatty acid levels in blood serum and is thought to induce insulin resistance. I56l... 

G.R. Fulcher, M. Walker, C. Catalano, I. Agius, and K. G.M.M. Alberti, Metabolic effects of suppression of non-esteri-fied fatty acid levels with acipimox in obese NIDDM subjects, Diabetes, 1992, 43, 1400-1408. 

Thyroid hormones enhance the lipolytic responses of fat cells to other hormones (e.g., catecholamines) and elevated plasma free fatty acid levels are seen in hyperthyroidism. Hyperthyroidism is an insulin resistant state, as manifested by depleted glycogen stores and enhanced gluconeogenesis this may precipitate diabetes mellitus or worsen glycemic control in diabetics on treatment. Conversely, insulin requirements are reduced in diabetics who become hypothyroid. 

Growth hozmone, glucose and free fatty acid levels in mother and Infant in normal, diabetic and tozamic pregnancies. 

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... 

The free fatty acids (FFA, nonesterified fatty acids, im-esterified fatty acids) arise in the plasma from hpolysis of triacylglycerol in adipose tissue or as a result of the action of hpoprotein hpase during uptake of plasma tri-acylglycerols into tissues. They are found in combination with albumin, a very effective solubilizer, in concentrations varying between 0.1 and 2.0 ieq/mL of plasma. Levels are low in the ftiUy fed condition and rise to 0.7-0.8 leq/mL in the starved state. In uncontrolled diabetes mellitus, the level may rise to as much as 2 Ieq/mL. 

Failure of mitochondria to oxidise fatty acids snfficiently rapidly reduces the ability of the muscle fibres and other cells to utilise fat after a meal, so that fat levels in the blood and in the muscle increase to abnormally high levels. Over a period of time, this disturbance can lead to obesity or type 2 diabetes meUitus (Chapter 9). 

The three fat fuels and their metabolism are involved directly or indirectly in diseases such as diabetes mellitus, syndrome X, obesity, atherosclerosis and coronary heart disease, which are discussed in other chapters in this book. This section considers the problems associated with high blood levels of ketone bodies and long-chain fatty acids. 

Although the cardiac side effects are considerably reduced, metabolic effects occur under the therapy with this /32-sympathomimetics increased plasma levels of free fatty acids, glucose and ketones. In diabetic patients a hyperglycaemic ketoacidosis can be induced. All /32-sympathomimetics reduce the potassium plasma level. 

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