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Review: low caloric intake and gall-bladder motor function.

Cholelithiasis is the primary expression of obesity in the hepatobiliary system. In obese subjects the risk of developing gallstones is increased due to a higher cholesterol saturation of gall-bladder bile. During weight reduction with very low calorie diets (VLCD) the incidence of gallstones increases, but the mechanism for gallstone formation is not completely understood and several pathogenetic mechanisms have been suggested: increased saturation of bile, increased gall-bladder secretion of mucin and calcium, increased presence of prostaglandins and arachidonic acid. Alterations in gall-bladder motility may contribute to gallstone formation, but few studies have addressed the issue of gall-bladder motility during rapid weight loss and its possible role in gallstone formation. VLCD have been associated with a gall-bladder stasis, as a consequence of reduced gall-bladder stimulation by low fat content of the diets. A threshold quantity of fat (10 g) has been documented to obtain efficient gall-bladder emptying. Ursodeoxycholic acid administered during VLCD seems to have a protective role in developing a biliary cholesterol crystals. Gall-bladder emptying was lower in response to low fat meals with respect to relative higher fat meals, before as well as during the VLCD. This may account the possibility of an adaptative response of the gall-bladder motility to a given diet regimen. Adequate fat content of the VLCD may prevent gallstone formation, maintaining adequate gall-bladder motility and may be more economic and physiologically acceptable than administration of a pharmacological agent.

Bile Acids and Salts↗

Associations of cardiovascular disease risk factors with measures of energy expenditure and caloric intake in a farm population.

The purpose of this study was to examine the relationships of several cardiovascular disease risk factors [blood pressure (BP), total cholesterol (TC), high-density-lipoprotein cholesterol (HDL-C), and the HDL-C:TC ratio], as well as the body mass index (BMI) and percent body fat with daily energy intake (EI) and daily energy expenditure (EE) of North Carolina farmers and their wives. Data were collected from 195 subjects. Daily EI and EE were estimated from 4-day food and 4-day activity records, respectively, collected on the same days. Pearson correlation coefficients for chronic disease risk factors with both EI and EE were generally low. When compared to EI, EE was more highly correlated with both lean body mass (r = 0.88) and BMI (r = 0.73), and was less time consuming and easier for the subjects to use. EE obtained from a reliable activity record may be a more practical tool for assessing the possible relationship(s) of energy metabolism to chronic disease risk factors.

Adult↗

Influence of caloric intake on aging and on the response to stressors.

Reducing the food intake of rodents to well below that of ad libitum fed animals increases the life span. This action, which gerontologists often refer to as the antiaging action of dietary restriction (DR), is due to the slowing of the aging processes. DR also maintains most physiological processes in a youthful state and delays the occurrence and/or slows the progression of age-associated disease processes. This antiaging action of DR results from the reduced intake of calories. Reduction of the body fat content does not play a causal role in the antiaging action of DR, nor does reduction in the metabolic rate. Alterations in the characteristics of carbohydrate metabolism and of oxidative metabolism in response to DR have been found that are of such a nature that they could, at least in part, underlie the antiaging action. Several theories have recently been proposed in regard to the mechanisms responsible for the antiaging action of DR, but none has been tested by rigorously designed studies. Of these theories, the one that seems most promising is based on the fact that DR protects rats and mice of all ages against the damaging actions of acute stressors. This protective action against stressors may play a major role in the antiaging action of DR.

Aging↗

Caloric intake alters the efficiency of catalase mRNA translation in the liver of old female mice.

The free radical theory of aging predicts that calorie restriction, which extends life span, should reduce oxidant damage. In mammals, the oxidative processes centered in the liver are a major source of free radicals. Liver catalase has the dominant role in the intracellular detoxification of hydrogen peroxide. In male rodents, published studies indicate that aging decreases catalase gene transcription and that calorie restriction obviates this effect. In females, published studies are inconsistent, and no molecular mechanisms have been identified. Here we report that, in female mice, aging can lead to an increase in the translational efficiency of hepatic catalase mRNA, and that calorie restriction obviates this effect. Consideration of these results and published studies leads us to propose that the variability in catalase results in females may arise from the small number of studies or from unique aspects of female physiology, perhaps the estrous cycle and its cessation with age.

Aging↗