Influence of nutrient intake on protein turnover (original) (raw)
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Energy contribution of proteins and lipids during prolonged fasting in the rat
Nutrition Research, 1991
It has previously been shown that there are many similarities between the metabolic responses during fasting in rats with large initial lipid reserves and man : in particular, they both withstand longterm fasting through an efficient sparing of body proteins. Three metabolic phases were characterized. However, to further elucidate the regulation of protein and lipid utilization, data were needed on the change in the contribution of these body fuels. We found that in rats, after the first two days (phase 13 , a steady state in protein utilization is reached (phase II). Proteins then account for only 17 % of energy expenditure whereas lipids provide the most important part, 83 %. There is thereafter a progressive rise in protein utilization (phase III).
American Journal of Physiology-Endocrinology and Metabolism, 2000
This study was undertaken to determine whether the protein feeding pattern could induce chronic adaptation of protein turnover. After a 15-day adaptive period, elderly (68 yr) and young (26 yr) women received, for 14 days, a diet providing 200 KJ ⋅ kg fat-free mass (FFM)− 1 ⋅ day− 1, where the daily protein intake (1.7 g protein ⋅ kg FFM− 1 ⋅ day− 1) was either spread over 4 meals in the spread pattern or mainly (80%) consumed at noon in the pulse pattern. One day after the end of the dietary treatment, whole body leucine kinetics were measured by use of a continuous [13C]leucine infusion, both in the postabsorptive state and in the same fed state. The pulse pattern was able to induce, in young as in elderly women, a lower postabsorptive leucine oxidation and endogenous leucine flux than the spread pattern and improved the responsiveness of nonoxidative leucine disposal during 4-h oral feeding. Thus the pulse pattern was able to induce chronic regulation of protein metabolism in you...
Relationships between lipid availability and protein utilization during prolonged fasting
Journal of Comparative Physiology B-biochemical Systemic and Environmental Physiology, 1992
Mammals and birds adapt to prolonged fasting by mobilizing fat stores and minimizing protein loss. This strategy ends with an increase in protein utilization associated with behavioural changes promoting food foraging. Using the Zucker rat as a model, we have investigated the effect of severe obesity on this pattern of protein loss during long-term fasting. Two interactions between the initial adiposity and protein utilization were found. First, protein conservation was more effective in obese than in lean rats: fatty rats had a three times lower daily nitrogen excretion and proportion of energy expenditure deriving from proteins, and a lower daily protein loss in various muscles. This phase of protein sparing is moreover nine times longer in the fatty rats. Second, obese animals did not show the late increase in nitrogen excretion that occurred in their lean littermates. Total body protein loss during starvation was larger in fatty rats (57% versus 29%) and, accordingly, total protein loss was greater in their muscles. At the end of the experiment, lean and obese rats had lost 98% and 82%, respectively, of their initial lipid reserves, and fatty rats still had an obese body composition. These results support the hypothesis that in severely obese humans and animals a lethal cumulative protein loss is reached long before the exhaustion of fat stores, while the phase of protein conservation is still continuing. In contrast, in lean rats, survival of fasting seems to depend on the availability of lipid fuels. The data also suggest that accumulation of too much fat in wild animals is detrimental for survival, because it eliminates the late phase of increase in nitrogen excretion that is linked to a food foraging behaviour anticipating a lethal depletion of body reserves.
The American Journal of Clinical Nutrition, 1997
We postulated whether interventions capable of restoring euglycemia would correct whole-body protein metabolism, shown previously to be elevated in hyperglycemic persons with non-insulin-dependent diabetes (NIDDM). The kinetics of protein metabolism were estimated in obese subjects with NIDDM in the hyper-and normoglycemic states during isoenergetic feeding and in the normoglycemic state induced by 4 wk of a very-low-energy diet (VLED) with constant protein intake. Seven NIDDM subjects [three males and four females with a body mass index (in kg/m2) of 39 ± 2] were given a weight-maintaining, liquid formula providing 95 g protein/d for 15 d, followed in six subjects (two males and four females) for 27 d by a diet providing 1 .7 Mi. 93 g protein derived from casein-soy, 13 g carbohydrate, 2 g fat, multivitamins and mmenals, and a potassium bicarbonate supplement (32 mmol) per day. Exogenous insulin was given to achieve normoglycemia during the first 8 d of isoenergetic feeding. On days 6-8, 12-14, and 25-27, nitrogen flux rate was calculated from the urine [ ' 5N]urea enrichment by using the 60-h oral ['5N]glycine method to obtain "integrated" feeding and fasting values. Rates of synthesis and breakdown were calculated from nitrogen flux. During isoenengetic feeding, normoglycemia was associated with more positive nitrogen balance (2.6 ± 0.5 compared with-0.6 ± 0.6 g N/d, P < 0.05): 18-23% lower nitrogen flux, and synthesis and breakdown rates (P < 0.05). and a 3% decrease in resting energy expenditure (P < 0.05). During the VLED, euglycemia was achieved but nitrogen balance, although it became less negative with time, never reached equilibrium. This was associated with significant (P < 0.05) decreases in the synthesis rate, resulting in net protein losses. Thus, the altered protein metabolism in moderately hyperglycemic NIDDM subjects was improved with exogenous insulin in doses sufficient to restore normoglycemia in the isoenergetic fed state, but it remained abnormal with a reduced nonprotein energy intake. This suggests that protein metabolism is more sensitive to insulinization than was thought previously.
Fed state protein metabolism in diabetes mellitus
The Journal of nutrition, 1998
Current knowledge concerning the physiologic regulation of protein anabolism during feeding is both limited and debated; little information is available on the effects of pathological conditions such as diabetes mellitus. This is due largely to methodological problems and the technical difficulties associated with the isotope dilution techniques used to estimate protein kinetics in the fed state. Data that are available suggest that meal intake induces protein anabolism in healthy subjects by reducing endogenous proteolysis and selectively stimulating protein synthesis, with amino acids and insulin playing the major regulatory role. Data obtained in subjects with noninsulin-dependent diabetes mellitus demonstrate that the impaired insulin action on glucose metabolism characteristic of that disease may not be associated with abnormal protein metabolism in the fed state. Severe insulin deficiency, as occurs in insulin-dependent diabetes, adversely affects nitrogen balance; at present,...
Turnover and recycling of glucose in man during prolonged fasting
Metabolism, 1977
The effect of prolonged (3-5 wk) fasting on tracer-determined glucose turnover and of recycling radioactive glucose has been examined. We followed the specific activity of plasma glucose after the simultaneous administration of 1 -"C-glucose and 3-3Hglucose. The rate of glucose turnover decreased during prolonged fasting. Recycling of radioactive glucose was estimated by two different techniques: ( 1) the appearance of "C in positions 2 to 6 glucose was measured;
Physiology & Behavior, 1985
Carbohydrate metabolism and .food intake in food-restricted rats. Relationship between the metabolic events during the meal and the degree of food intake. PHYSIOL BEHAV 35(5) 695-700, 1985.-To study some metabolic features during feeding in food-restricted rats two groups of animals were maintained on a 2 hr feeding/22 hr fast schedule. Group D (n=38) received a meal every day from 8:00 to 10:00 a.m. Group N (n=34) was given the meal from 8:00 to 10:00 p.m. The average total amount of food ingested by rats of group N in the two hour period was 6.3-0.4 whereas Group D ingested 4.8_+0.3 g/100 g b.w. The metabolic pattern also was different in one group as to the other. The basal liver glycogen content when feeding started was considerably lower in the nocturnal group (0.14_+0.02 mg/100 mg of liver tissue) than in the diurnal group (0.44_+0.10 mg/100 nag). Afterwards glycogen increased in both groups but more steeply and intensely in group N. Glycemia increased in group D and was almost invariant in group N. Insulinemia went up in both groups but in group D its peak was higher and occurred 60 minutes after the onset of feeding whereas the peak in group N was much lower and occurred at 90 minutes. There was a clear dissociation between the time courses ofinsulinemia and glycemia in both groups, especially in group N, which suggests a central control of insulin secretion during feeding that partially unlocks it from blood glucose concentration. The hepatic glycogen content was partially linked to the amount of food ingested but again there was a dissociation between these two variables, inasmuch as a higher glycogen replenishment in the nocturnal group corresponded to a larger food intake. Carbohydrate metabolism Food intake Metabolic events during a meal Food-restriction