Adipose tissue, carbohydrate metabolism

Fat is the major way we store energy. Fat is stored principally in adipose tissue and can be stored in virtually unlimited amounts. Fat is metabolized through (1 oxidation to acetyl-CoA and then through the TCA cycle, where it s burned completely to C02 to make ATP. Fat cannot be used to make carbohydrate because acetyl-CoA cannot be converted directly to precursors of glucose without losing its carbon atoms first (you ll see what this really means later). 

Lipid metabolism in the liver is closely linked to the carbohydrate and amino acid metabolism. When there is a good supply of nutrients in the resorptive (wellfed) state (see p. 308), the liver converts glucose via acetyl CoA into fatty acids. The liver can also take up fatty acids from chylomicrons, which are supplied by the intestine, or from fatty acid-albumin complexes (see p. 162). Fatty acids from both sources are converted into fats and phospholipids. Together with apoproteins, they are packed into very-low-density lipoproteins (VLDLs see p.278) and then released into the blood by exocytosis. The VLDLs supply extrahepatic tissue, particularly adipose tissue and muscle. 

Il.f.l.1. Insulins. Insulin is the most effective of diabetes medications. Insulin has profound effects on carbohydrate, protein, fat metabolism and electrolytes. It has anabolic and anticatabolic actions. In a state of insulin deficiency, glycogenesis, glucose transport, protein synthesis, triglyceride synthesis, LPL activity in adipose tissue, cellular potassium uptake all decrease on the other hand, gluconeogene-sis, glycogenolysis, protein degradation, ketogene-sis, lipolysis increase. 

Fatty acids stored in adipose tissue, in the form of neutral TAG, serve as the body s major fuel storage reserve. TAGs provide concentrated stores of metabolic energy because they are highly reduced and largely anhydrous. The yield from complete oxidation of fatty acids to CO2 and H2O is nine kcal/g of fat (as compared to four kcal/g of protein or carbohydrate, see Figure 27.5, p. 357). 

GH administered to hypophysectomized rats in vivo causes a drop in the level of plasma non-esterified fatty acids (NEFA), followed by a prolonged increase in this level [89]. This appears to be due to increased utilization of lipids - increased uptake of NEFA by muscle preceding increased output by adipose tissue. As a consequence GH diverts the energy metabolism of the organism from carbohydrate utilization to lipid utilization, and acts to oppose the effects of insulin. Actions of GH on lipid metabolism are particularly marked in man, where GH levels become elevated on fasting and presumably serve to help stimulate the increased lipid utilization seen in this condition. In contrast, in the rat, GH levels fall on fasting. 

Human growth hormone hGH Liver, adipose tissue Promotes growth lipid and carbohydrate metabolism... 

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