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Carbohydrate starvation

However, every molecule of acetoacetic add or its derivatives that the liver accumulates and subsequently excretes means that two potential acetyl-CoA molecules have not been exploited so as to release their potential energy through oxidation by way of the citric add cycle. Why Particularly as fatty acid oxidation only occurs under conditions of carbohydrate starvation, one may well... [Pg.164]

Glucose metabolism is controlled differently In various mammalian tissues to meet the metabolic needs of the organism as a whole. During periods of carbohydrate starvation, for instance, glycogen In the liver Is converted directly to glucose 6-phosphate (without Involvement of hexokinase). Under these conditions, there Is a reduction in fructose 2,6-bisphos-... [Pg.314]

In this study we used following microorganisms lyophilized probiotic cultures of E. coli M-17, Bifidobacterium bifidum, Lactobacillus acidophilus and three nisin producing strains of Lactococcus lactis ssp. lactis MSU, 729 and F-116 that were incubated in carbohydrate starvation conditions [2] and contained more than 99.9% noneulturable cells. [Pg.336]

Ganesan, B., Stuart, M.R., and Weimer, B.C. (2007) Carbohydrate starvation causes a metabolically active but noncultuiable state in Lactococcus lactis. Appl Environ Microbiol 73, 2498-2512. [Pg.336]

The first hormonal signal found to comply with the characteristics of both a satiety and an adiposity signal was insulin [1]. Insulin levels reflect substrate (carbohydrate) intake and stores, as they rise with blood glucose levels and fall with starvation. In addition, they may reflect the size of adipose stores, because a fatter person secretes more insulin than a lean individual in response to a given increase of blood glucose. This increased insulin secretion in obesity can be explained by the reduced insulin sensitivity of liver, muscle, and adipose tissue. Insulin is known to enter the brain, and direct administration of insulin to the brain reduces food intake. The adipostatic role of insulin is supported by the observation that mutant mice lacking the neuronal insulin receptor (NDRKO mice) develop obesity. [Pg.209]

Figure 8. A. Glycogen content in the vastus lateralis muscle after a mixed diet (a) and during 5 days of total starvation ( ) in one subject and eight days of carbohydrate-poor diet (o) followed by a carbohydrate-rich diet ( ) in a second subject. B. Muscle glycogen content before and after exercise. Before exercise the diet was mixed (a) and in the following days was either total starvation ( ) or carbohydrate-poor (o) and finally followed by 1-2 days of a carbohydrate-rich diet ( ). Note the slow rate of glycogen resynthesis when the diet is carbohydrate-poor compared to the rate when the diet is carbohydrate-rich. Redrawn from Hultman and Bergstrom (1967). Figure 8. A. Glycogen content in the vastus lateralis muscle after a mixed diet (a) and during 5 days of total starvation ( ) in one subject and eight days of carbohydrate-poor diet (o) followed by a carbohydrate-rich diet ( ) in a second subject. B. Muscle glycogen content before and after exercise. Before exercise the diet was mixed (a) and in the following days was either total starvation ( ) or carbohydrate-poor (o) and finally followed by 1-2 days of a carbohydrate-rich diet ( ). Note the slow rate of glycogen resynthesis when the diet is carbohydrate-poor compared to the rate when the diet is carbohydrate-rich. Redrawn from Hultman and Bergstrom (1967).
Figure 9. One-legged exercise studies showing the muscle glycogen content of the exercised (—) and rested legs (—) in two subjects. A. Muscle biopsy samples were obtained immediately after exercise (a) and during three days when fed a carbohydrate-rich diet (a). B and C. The diet was total starvation (z) for two days following exercise (B) or carbohydrate-poor (o) for three days following exercise (C). This was followed by a second one-leg exercise bout (T) and a carbohydrate-rich diet ). Redrawn from Bergstrom and Hultman (1966) in panel A, and from Hultman and Bergstrom (1967) in panels B and C. Figure 9. One-legged exercise studies showing the muscle glycogen content of the exercised (—) and rested legs (—) in two subjects. A. Muscle biopsy samples were obtained immediately after exercise (a) and during three days when fed a carbohydrate-rich diet (a). B and C. The diet was total starvation (z) for two days following exercise (B) or carbohydrate-poor (o) for three days following exercise (C). This was followed by a second one-leg exercise bout (T) and a carbohydrate-rich diet ). Redrawn from Bergstrom and Hultman (1966) in panel A, and from Hultman and Bergstrom (1967) in panels B and C.
Nilsson, L.H. Hultman, E. (1973). Liver glycogen in man. The effect of total starvation or a carbohydrate-poor diet followed by carbohydrate refeeding. Scand. J. Clin. Lab. Invest. 32, 325-330. [Pg.278]

Inherited aldolase A deficiency and pyruvate kinase deficiency in erythrocytes cause hemolytic anemia. The exercise capacity of patients with muscle phos-phofiaictokinase deficiency is low, particularly on high-carbohydrate diets. By providing an alternative lipid fuel, eg, during starvation, when blood free fatty acids and ketone bodies are increased, work capacity is improved. [Pg.143]

The basic form of ketosis occurs in starvation and involves depletion of available carbohydrate coupled with mobihzation of free fatty acids. This general pattern of metabohsm is exaggerated to produce the pathologic states found in diabetes meUitus, twin lamb disease, and ketosis in lactating catde. Nonpathologic forms of ketosis are found under conditions of high-fat... [Pg.188]

The calorific capacity of amino acids is comparable to that of carbohydrates so despite their prime importance in maintaining structural integrity of cells as proteins, amino acids may be used as fuels especially during times when carbohydrate metabolism is compromised, for example, starvation or prolonged vigorous exercise. Muscle and liver are particularly important in the metabolism of amino acids as both have transaminase enzymes (see Figures 6.2 and 6.3 and Section 6.4.2) which convert the carbon skeletons of several different amino acids into intermediates of glycolysis (e.g. pyruvate) or the TCA cycle (e.g. oxaloacetate). Not all amino acids are catabolized to the same extent... [Pg.254]

Another, perhaps less dramatic condition, is the effect of social drinking after a very short period of starvation. A period of eating a high protein, low carbohydrate meal for several days, followed by a missed breakfast and a late lunch might result in a low level of liver glycogen. If now, lunch is preceded by alcoholic drinks, hypoglycaemia could readily develop, and, if severe, could lead to coma with possible... [Pg.116]

The plasma concentration of ketone bodies in fed, healthy humans is very low (about 0.1 mmol/L) so that the rate of utilisation is very low. However, it is elevated in several conditions, e.g. starvation, hypoglycaemia, affer physical activity. In starvation in normal adults, it increases to about 3 mmol/L after three days and to 5-6 mmol/L after several more days (Figure 7.24). Nevertheless, it can increase to 3 nunol/L or higher within a few hours of completing a prolonged period of physical activity if food, particularly carbohydrate, is not eaten (known as accelerated starvation ) (Table 7.3). Ketone bodies are particularly important in children, since starvation can quickly result in severe hypoglycaemia. This is due to the fact that the amount of glycogen stored in the liver of a child is... [Pg.144]

The use of prolonged starvation for treatment of obesity has posed a fascinating problem that man is capable of fasting for periods of time beyond which he would have used all his carbohydrate resources and all his protein for gluconeogenesis in order to provide adequate calories as glucose for the central nervous system. [Pg.363]

Table 16.1 Energy provided from the oxidation of carbohydrate, fat and protein after 12 and 60 hours starvation in normal lean subjects... Table 16.1 Energy provided from the oxidation of carbohydrate, fat and protein after 12 and 60 hours starvation in normal lean subjects...
Since the presumed cytosolic pathway interfaces directly with the network of secondary metabolism, the observed induction of DS-Co and CM-2 isozymes in response to wounding was expected. However, the even greater response of plastidic isozymes was unexpected. Perhaps the increased pull on carbohydrate metabolism in the cytosol affects the balance of substrates feeding into the aromatic pathway of the plastid. If so, a tendency to starvation for pathway endproducts may trigger derepression of the plastidic-pathway isozymes. [Pg.105]

During starvation or in uncontrolled diabetes mel-litus, when carbohydrates are either unavailable or not properly utilized, cellular proteins are used as fuel. [Pg.656]


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Starvation

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