Energy metabolism fasting

Carnitine is a vitamin-like quaternary ammonium salt, playing an important role in the human energy metabolism by facilitating the transport of long-chained fatty acids across the mitochondrial membranes. An easy, fast, and convenient procedure for the separation of the enantiomers of carnitine and 0-acylcarnitines has been reported on a lab-made teicoplanin-containing CSP [61]. The enantioresolution of carnitine and acetyl carnitine was enhanced when tested on a TAG CSP, prepared in an identical way [45]. Higher a values were reached also in the case of A-40,926 CSP [41]. 

The primary role of liver in energy metabolism during fasting is the syr thesis and distribution of fuel molecules for use by other organs. Thus one speaks of "hepatic metabolism" and "extraheptic" or "peripheral metabolism. 

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. 

The hormonal picture, as far as glucagon and insulin are concerned, is similar during exercise and fasting. The concentration of plasma glucagon increases during both states, and this elevation stimulates the synthesis of cAMP in cells and the phosphorylation of various enzymes involved in energy metabolism. The arrays of enzymes that become phosphorylated are largely identical for both conditions, and the resultant patterns of activation or inactivation of enzymes are similar or identical. 

Anabolic steroids decrease catabolism and increase skeletal muscle protein synthesis. Whether this results in muscular hypertrophy or hyperplasia, or a combination of these, is unclear and probably depends upon the muscle studied. Different muscle types contain different cytosolic receptor numbers and, therefore, the response to anabolic steroids varies. Anabolic steroids initiate an increase in RNA polymerase activity and the synthesis of either structural or contractile proteins. In some muscles, anabolic steroids may increase the ratio of fast twitch to slow twitch fibers (Nimmo et al 1982, Snow et al 1982). Increased activity of enzymes involved in energy metabolism may also occur. However, the total glycogen content may remain unchanged (Hyyppa et al 1997). The effects are most profound in females and castrated males (Snow 1993). 

Protection from hypoxia in fasted animals (mildly ketotic) resulted in improved survival time and a reduction in lactic acid prodnction without a generalized redaction in cerebral energy metabolism. It was snggested that this protection was dne to... 

There are many ways to categorize inborn errors of metabolism. When considering the effectiveness of therapeutic procedures in acute illness, metabolic disorders can be classified into five groups (1) disorders presenting with intoxication syndrome, (2) disorders of reduced tolerance to fasting, (3) disorders of mitochondrial energy metabolism, (4) disorders of neurotransmission, and (5) disorders with limited therapeutic options in illness [8],... 

Bimie J.W., R.E. Agnew and F.J. Gordon, 2000. The influence of body condition on the fasting energy metabolism of nonpregnant, nonlactating dairy cows. J. Dairy Sci. 83, 1217-1223. 

It is possible, of course, to use direct calorimetry, often in combination with the indirect approach (OUR) to investigate the properties of muscle under different physiological conditions and in the diseased state. Chinet s group [70] found that the slow- and fast-twitch skeletal muscle fibres from the murine model of Duchenne muscular dystrophy had a reduced sarcoplasmic energy metabolism as measured by the combined direct and indirect calorimeter [69]. The possibility that this could be due to diminished glucose availability was then examined [71] but was dismissed in favour of decreased oxidative utilisation of glucose and free fatty acids, conceivably due to defective mitochondria. 

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