Effects of fasting therapy in obese dogs on body weight, and hematological, blood coagulation and serum biochemical values

Body weight, hematological parameters, blood coagulation profiles and serum biochemistry values were investigated in obese beagles during the fasting and refeeding period. There were no severe clinical changes (alopecia, hepatopathy, respiratory abnormalities and cardiac sufficiency) in the obese dogs throughout this study. During refeeding the obese dogs showed two phases of weight reduction - initial rapid weight loss and subsequent slow weight loss. After refeeding, they rapidly regained their initial body weight. Except for transient decreases in some erythrocytic parameters, fasting therapy had no apparent effects on hematological and blood coagulation values. Serum biochemical examinations revealed significant changes in fasting period. In carbohydrate metabolism, blood glucose concentrations gradually decreased and insulin levels declined to normal range. Total ketone body levels rose mainly due to increases in 3-hydroxybutyrate concentrations. In lipid metabolism, triglyceride, total cholesterol and phospholipids decreased and fatty acid values. The enzyme activities varied within the normal limits. These serum biochemical parameters recovered to the initial levels immediately after the beginning of refeeding. These clinical and clinicopathological results reveal that obese dogs tolerate fasting very well without developing severe ketosis. Our data suggested that obese dogs could use very efficiently ketone bodies and free fatty acids for energy requirements during fasting. In conclusion, fasting therapy does not cause any adverse effects (anemia, severe ketosis and behavioural abnormailities) in obese dogs.

Effects of fasting therapy in obese dogs on body weight, and hematological, blood coagulation and serum biochemical values

Body weight, hematological parameters, blood coagulation profiles and serum biochemistry values were investigated in obese beagles during the fasting and refeeding period. There were no severe clinical changes (alopecia, hepatopathy, respiratory abnormalities and cardiac sufficiency) in the obese dogs throughout this study. During refeeding the obese dogs showed two phases of weight reduction - initial rapid weight loss and subsequent slow weight loss. After refeeding, they rapidly regained their initial body weight. Except for transient decreases in some erythrocytic parameters, fasting therapy had no apparent effects on hematological and blood coagulation values. Serum biochemical examinations revealed significant changes in fasting period. In carbohydrate metabolism, blood glucose concentrations gradually decreased and insulin levels declined to normal range. Total ketone body levels rose mainly due to increases in 3-hydroxybutyrate concentrations. In lipid metabolism, triglyceride, total cholesterol and phospholipids decreased and fatty acid values. The enzyme activities varied within the normal limits. These serum biochemical parameters recovered to the initial levels immediately after the beginning of refeeding. These clinical and clinicopathological results reveal that obese dogs tolerate fasting very well without developing severe ketosis. Our data suggested that obese dogs could use very efficiently ketone bodies and free fatty acids for energy requirements during fasting. In conclusion, fasting therapy does not cause any adverse effects (anemia, severe ketosis and behavioural abnormailities) in obese dogs.

Starvation reduces renal pyruvate dehydrogenase phosphate phosphatase activity - abstract

We have measured the rates of activation of the mitochondrial pyruvate dehydrogenase multi-enzyme complex (PHD) in kidney mitochondria from fed and starved rats. A significant diminution of rate due to starvation was found. The effect of varying Mgý+ concentration on the rate suggests that starvation induced a covalent modification of PDH phosphatase or its substrate which modification impaired dephosphorylation by decreasing its sensitivoty to Mgý+ (AU)

Protein deficiency, energy deficiency, and the oedema of malnutrition

The role of dietary protein deficiency in kwashiorkor is uncertain, although it has been shown not to be involved in the famine oedema of adults. A study of six different diets given to 103 children with oedematous malnutrition showed that the rate of loss of oedema was strongly correlated with the dietary energy intake (r=-0.75) but not with the protein intake (r=0.03). 66 patients given a very-low protein diet (2.5 percent protein energy) lost oedema as fast as those given five times as much protein. The energy intake above which oedema accumulated was 245-270 KJ/kg/day. Because energy deficiency is not invariably associated with oedema it cannot be the only factor involved, and the other necessary dietary component(s) must therefore have been present in surfeit in all the therapeutic diets. This could be potassium together with factors necessary for its retention. The accessory ingredients must be low in foods associated with human and experimental nutritional oedema. It is suggested that protein deficiency is not the cause of the oedema of kwashiorkor and that there is no need to postulate a different pathogenesis for this oedema from starvation oedema of adults. (Summary)

Biochemical aspects of ketogenesis, a review

Ketogenesis occurs only under certain physiological conditions, the physiological substrate for the process being long chain fatty acids. The condition for ketogenesis arises if the long chain fatty acid levels are high enough to render the liver incapable of metabolising all the acetyl CoA, formed as a result of hepatic oxidation of long chain fatty acids, via the tricarboxylic acid cycle to yield water and carbon dioxide. The state in which unesterified fatty acid levels are high enough to cause ketogenesis can be arrived at if there is a lack of insulin or a condition of starvation. Biochemical regulation, pathological condition and relative levels of ketone bodies are also reviewed. It was found that maximum ketonemia reflects not only increased production but also decreased use. The determination of urine or plasma 3-hydroxybutyrate may be of more importance than a simple urinary test upon ketone bodies in diabetic persons

Ammonia production by the small intestine of the rat

Slices of duodenum and jejunum produce ammonia from glutamine in vitro. Ammoniagenesis does not increase in response to acidosis or potassium deficiency, two conditions known to cause enhanced ammoniagenesis in the kidney. Gut contains glutamine 1 as well as ç-glutamyl transpeptidase. These enzymes do not show any increase during starvation (SUMMARY)

Effect of starvation on renal metabolism in the rat

The effects of starvation an the acid base status of the rat and on the gluconeogenic and ammoniagenic capacity of rat renal-cortical slices were examined. Starvation for 48 or 72 hrs did not affect acid-base status, and urinary ammonia production did not change. Kidney cortical slices from starved as compared to fed rats showed increased gluconeogenic capicity when incubated with the substrated pyruvate, succinate, fumarate, malate, 2-oxoglutarate, glutamine and glutamate. Renal cortical tissues from starved rats also had increased activity of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase. Renal cortical slices from starved rats did not differ from those of fed rats in the ability to produce ammonia from glutamine or glutamate, nor was there any difference in the activity of glutaminase between these groups. These results show that renal gluconeogenic capacity is increased in starved rats in the absence of systemic acidosis, and starvation does not lead to an increase in urinary ammonia excretion or renal ammoniagenic capacity. (AU)

Control of renal cortex ammoniagenesis and its relationship to renal cortex gluconeogenesis

The metabolism of glutamate by kidney cortical slices from normal and acutely acidotic rats and the effect of acidosis in vitro on the metabolism of these two substrates has been investigated. The effects of calcium on all these processes was also studied. Kidney cortical slices from acutely acidotic rats utilized more glutamine and formed more ammonia, glucose and glutamate than slices from rats. Increased glutamine utilization and ammoniagenesis by cortical slices from acidotic rats was not detected when Ca2+ was omitted from the medium, although glucose formation was still enhanced and glutamate formation decreased. With in vitro acidosis there was no change in glutamine uptake in the presence or absence of calcium but with calcium, ammonia production fell. Although there was no change in glutamate uptake by cortical slices from acidotic rats, there was an increase in ammoniagenesis and gluconeogenesis with or without calcium. With in vitro acidosis the only significant changes were an increase in ammoniagenesis and gluconeogenesis in the absence of calcium. The results show that ammoniagenesis from glutamine is controled by a rate-limiting step distinct from that which controls deamination of glutamate and gluconeogenesis from glutamine and glutamate. Possible control points and the interrelationship between ammoniagenesis and gluconeogenesis are discussed (AU)

The protective effects of feeding on the hepatic ultrastructure of rats treated with hypoglycin

Hypoglycin is a toxic amino acid found in the fruit of the unripe ackee (Blighia sapida), and associated with Jamaican "vomiting sickness". It produces profound hypoglycaemia when administered to starved rats, and this is accompanied by gross mitochondrial swelling in liver cells. This ultrastructural change is reduced or absent in animals that have been allowed to feed ad libitum, provided that normal blood glucose levels are maintained. Mitochondrial swelling is not a feature of acute hypoglycaemia induced by insulin, under the conditions of this experiment.(AU)

Protein turnover in skeletal muscle. I. The effect of starvation and a protein-free diet on the synthesis and catabolism of skeletal muscle proteins in comparison to liver

Rates of synthesis and catabolism of liver and muscle sarcoplasmic and myofibrillar protein have been measured in young control, starved and protein (deprived) rats using [14C]Na2CO3 to label protein. Half-lives for synthesis of 1.35, 2.8 and 7.2 days for liver, sarcoplasmic and myofibrillar proteins, respectively were obtained, whilst half-lives for catabolism were 1.55, 3.6 and 15.6 days in each case in the control animals. The protein free diet for 3 days caused a small decrease in the rate of synthesis of liver and muscle proteins. The catabolic rate of liver protein was increased by 20 percent whilst there was a smaller increase in the catabolic rate of myofibrillar proteins. Starvation for 3 days caused a 20 percent reduction in the rate of liver protein synthesis whilst there were greater reductions in muscle protein synthesis. The catabolic rate of liver protein was only slightly increased whereas there was a 75 percent increase in the rate of myofibrillar protein breakdown. The total amount of protein synthesis and catabolism in liver and the 2 muscle protein fractions over the first 3 days of the 3 regimes were calculated. Muscle protein turnover, in particular myofibrillar, was shown to be very sensitive to dietary protein and/or calorie deficiency. These results are discussed in terms of the mobility and therefore importance of muscle protein metabolism in the economy of the whole animal. (AU)