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At least 577 records · Page 32Linked to original sources
PubMed1985

Glycemic effects of intensive caloric restriction and isocaloric refeeding in noninsulin-dependent diabetes mellitus.

To assess the effects of very low caloric (VLC) diets on glucose homeostasis in noninsulin-dependent diabetes mellitus, 30 obese subjects with NIDDM were studied for 40 days while eating a 330 Cal/day diet, with a subgroup of 12 subjects further evaluated during 40 days of refeeding. All subjects successfully lost weight, with an average weight loss of 4.6 +/- 0.2 kg (+/- SEM) after 10 days, 7.1 +/- 0.3 kg after 20 days, and 10.5 +/- 0.4 kg after 40 days of VLC diet therapy. Thus, weight loss was steady and progressive throughout the diet period. In contrast, the majority (87%) of the reduction in mean fasting plasma glucose (FPG) levels (297 +/- 13 to 158 +/- 10 mg/dl; P less than 0.001) occurred after 10 days of VLC diet therapy, with a further reduction in glucose levels to 138 +/- 9 mg/dl on day 40. The FPG response measured after 10 days of VLC diet was unrelated to the degree of obesity, rate or extent of weight loss, or prevailing insulin levels, but did correlate significantly with the initial FPG level (r = 0.37; P less than 0.05) and duration of diabetes (r = 0.42; P less than 0.05). After discontinuation of the VLC diet and refeeding of an isocaloric (weight maintenance) diet in 12 subjects, a variable increase in the FPG occurred, with an average increase of 80% after 40 days of refeeding. However, the mean FPG level after 40 days of refeeding was still markedly lower than that before VLC diet therapy (254 +/- 20 vs. 167 +/- 14 mg/dl; P less than 0.02) despite withdrawal of antidiabetic medication in all subjects. The basal hepatic glucose output (HGO) fell rapidly from 149 +/- 13 to 81 +/- 5 mg/M2 X min (P less than 0.001) after 10 days of VLC diet and rose from 67 +/- 4 to 88 +/- 7 mg/M2 X min (P less than 0.001) after 10 days of refeeding. Basal HGO demonstrated a highly significant positive correlation with FPG levels (r = 0.89; P less than 0.001) before and during both VLC diet therapy and refeeding. A significant correlation was also found between the change in FPG level and the change in basal HGO (r = 0.84; P less than 0.001) during both VLC diet and refeeding. Compared to that before the VLC diet, glucose tolerance to mixed meals was markedly improved during the refeeding period, with no change in circulating insulin levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMedDate not supplied

Neuroendocrine involvement in aging: evidence from studies of reproductive aging and caloric restriction.

Neuroendocrine changes contribute to female reproductive aging, but changes in other tissues also play a role. In C57BL/6J mice, neuroendocrine changes contribute to estrous cycle lengthening and reduced plasma estradiol levels, but the midlife loss of cyclicity is mainly due to ovarian failure. Hypothalamic estrogen receptor dynamics and estrogenic modulation of gene expression are altered in middle-aged cycling mice. Although insufficient to arrest cyclicity, these neuroendocrine changes may contribute to other reproductive aging phenomena, such as altered gonadotropin secretion and lengthened estrous cycles. In women, the loss of ovarian oocytes, the cause of menopause, accelerates in the decade before menopause. Accelerated oocyte loss may in turn be caused by a selective elevation of plasma follicle stimulating hormone, and neuroendocrine involvement may thus be implicated in menopausal oocyte loss. Chronic calorie restriction retards both neural and ovarian reproductive aging processes, as well as age-related change in many other physiological systems. The diverse effects of food restriction raises the possibility of an underlying coordinated regulatory response of the organism to reduced caloric intake, possibly effected through alterations of neural and/or endocrine signalling. We are therefore attempting to identify neuroendocrine changes that may coordinate the life prolonging response of animals to food restriction. Our initial focus is on the glucocorticoid system. Food restricted rats exhibit daily periods of hyperadrenocorticism, manifest as elevated free corticosterone during the diurnal peak. We hypothesize that this hyperadrenocortical state potentiates cellular and organismic homeostasis throughout life in a manner similar to that achieved during acute stress, thereby retarding aging processes and extending life span.

Aging↗
PubMed1990

Modifications of abdominal fat and hepatic insulin clearance during severe caloric restriction.

Using computed tomography on 19 obese female subjects, we determined abdominal adipose tissue, both subcutaneous and visceral adipose tissue, before and after 2 weeks of a very low caloric diet (VLCD). The following parameters were also determined before and after 15-20 days of VLCD: plasma glucose and insulin levels, oral glucose tolerance test, basal pancreatic insulin secretion estimated by fasting C peptide (Cp), and fasting insulin hepatic clearance calculated by Cp/insulin molar ratio. After VLCD the body weight and body mass index significantly declined (p less than 0.01); whereas abdominal adipose tissue and visceral abdominal tissue (VAT) significantly decreased (p less than 0.01), modifications of subcutaneous abdominal tissue (SAT) were not significant. Fasting insulin levels and plasma glucose response to oral glucose load significantly decreased (p less than 0.05). Insulin response remained unchanged. Cp immunoreactive insulin (IRI) significantly increased (p less than 0.01). A significant positive correlation was found between delta VAT and delta Cp/IRI before and after VLCD (p less than 0.01). Our data seem to suggest that the weight loss induced by VLCD fundamentally involves a decrease in VAT. The reduction in visceral fat could be associated with an increase in hepatic insulin clearance.

Abdomen↗
PubMed1987

Gonadal regression induced by caloric restriction is not mediated by the pineal gland in deer mice (Peromyscus maniculatus).

The role of the pineal gland in mediating reproductive regression in response to nonphotoperiodic cues was assessed. A proportion of deer mice (Peromyscus maniculatus) undergo gonadal regression subsequent to moderate food restriction. The reproductive regression after inanition qualitatively and quantitatively resembles short-day-induced regression. The physiological mechanisms responsible for gonadal regression after food restriction are unknown. The hypothesis that the mechanisms underlying photoperiodic responsiveness also mediate testicular regression caused by reduced food consumption was tested. Males were pinealectomized or received sham operations. Upon recovery, food availability was restricted to 70% of ad libitum intake. After 8 weeks, the reproductive condition was examined. Pinealectomy did not prevent gonadal regression, suggesting that the pineal gland does not mediate caloric information in this species.

Animals↗
PubMed2003

Influence of apolipoprotein E genotype on the response to caloric restriction in type 2 diabetic patients with hyperlipidaemia.

AIMS: Hyperlipidaemia is a major predisposing factor to atherosclerosis in patients with type 2 diabetes. Apolipoprotein (apo) E polymorphism influences lipoprotein metabolism, and the present study was undertaken to explore the relation, in type 2 diabetics, between apo E genotype and the plasma lipid response to dietary therapy. METHODS: The subjects were 104 patients with type 2 diabetes and hyperlipidaemia, and the difference, due to apo E genotype, in dietary response was followed for 4-6 weeks. The caloric intake was maintained in the range 20-25 kcal/kg, and the medications for diabetes were not changed during the follow-up period. RESULTS: Plasma total cholesterol (TC) and triglyceride (TG) levels were significantly lowered by the dietary treatment in patients with apo E genotypes of epsilon3/3, epsilon2/3 and epsilon3/4; however, the lipid levels in patients with epsilon2/4 did not respond to the diet. CONCLUSIONS: apo E genotype should be taken into consideration in the treatment of hyperlipidaemia in diabetic patients.

Adult↗
PubMed1992

Effects of alcohol and caloric restrictions on blood pressure and serum lipids in overweight men.

We have examined the independent and combined effects on blood pressure and blood lipids of alcohol restriction and weight loss in overweight male drinkers with a view to assessing overall effects on cardiovascular risk of two widely promoted nonpharmacological approaches for hypertension. Eighty-six men with a mean age of 44.3 years, a mean regular alcohol intake of 440 ml/wk (five or six standard drinks per day), a mean blood pressure of 137.4 mm Hg systolic and 84.8 mm Hg diastolic, and a mean body mass of 92.5 kg entered a controlled two-way factorial study. The subjects were randomly assigned to four groups for an 18-week intervention in which members of two groups drank only low-alcohol beer, thereby reducing their alcohol intake by 374 ml/wk, while those of the other two groups continued their normal alcohol intake. Within the low and normal alcohol intake groups subjects either continued their usual diet or reduced their caloric intake by 4,200-6,300 kJ/day (1,000-1,500 kcal/day) (with protein, fat, and carbohydrate provided as 15%, 30%, and 55% of total calories, respectively). Calorie reduction and alcohol restriction caused weight losses of 7.5 (p less than 0.001) and 2.1 (p less than 0.01) kg, respectively. Calorie reduction and alcohol restriction were associated with decreases in systolic blood pressure of 5.4 (p less than 0.001) and 4.8 (p less than 0.01) mm Hg, respectively, and in diastolic blood pressure of 4.2 (p less than 0.001) and 3.3 (p less than 0.01) mm Hg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Possible mechanisms underlying the antiaging actions of caloric restriction.

Restricting the food intake of mice and rats to well below that of ad libitum-fed animals markedly slows the aging processes. This action is reflected in an increase in longevity, a decrease in the age-associated increase in age-specific mortality rate, the maintenance of the physiological processes in a youthful state even at advanced ages, and the delaying of the onset or slowing of the progression or both of most age-associated diseases. The dietary factor responsible is the reduction in energy (caloric) intake. Many hypotheses have been proposed regarding mechanisms underlying this antiaging action. Hypotheses relating the antiaging action to the retardation of growth and development, the reduction of adipose mass, and the reduction of metabolic rate have been found to be wanting. Two of the proposed hypotheses have some evidence in their support. One involves the altered metabolic characteristics of glucose fuel use and of oxidative metabolism. The other relates to the enhanced ability of the rodents restricted in food intake to cope with challenges, which in turn has been linked to the glucocorticoid system and to the heat-shock protein system.

Aging↗
PubMed1984

Effect of nutritional status on the lung surfactant system: food deprivation and caloric restriction.

It has been reported that food deprivation may result in decreased synthesis of lung surfactant phospholipids while the ratio of saturated and unsaturated fatty acids of phosphatidylcholine is maintained. To further investigate this effect, rats were deprived of diet for 24, 48, 72, or 96 hr or fed a nutritionally complete but calorie-deficient diet for 48, 96, 144, and 192 hr. The surfactant was separated into extracellular and intracellular fractions, with the remaining lung tissue pooled as a nonsurfactant fraction. The total phospholipids, phosphatidylcholine, phosphatidylglycerol, and disaturated phosphatidylcholine of each surfactant fraction and the remaining lung tissue were analyzed. The data suggest that on a DNA basis, food and caloric deprivation results temporarily in an altered quantity of pulmonary phospholipids. By 96 hr of fasting or 192 hr of calorie-deficient diet, the pool sizes were replenished and no longer significantly different from the control state. In addition, the distribution of phosphatidylglycerol and phosphatidylcholine was modified in extracellular and intracellular surfactant fractions and in the nonsurfactant tissue fraction. Although the percentage of total phospholipids found as phosphatidylcholine was decreased, the relationship between saturated and unsaturated phosphatidylcholine was preserved in the extracellular surfactant fraction. These results demonstrate that during food and caloric deprivation, the lung quickly adapts to maintain the quality and quantity of surfactant on the alveolar surface.

Animals↗
PubMed1992

Caloric restriction in gestational diabetes mellitus: when and how much?

Variations in nutritional intake during pregnancy have measurable effects on the circulating levels of maternal nutrients, maternal weight gain, and birth weight of the offspring. A growing body of evidence indicates that alterations in maternal metabolism can also have long-term consequences in the offspring in relation to adult adiposity, glucose tolerance, and perhaps intellectual development. Therefore, recommendations for diet during pregnancy must be made with great care, and with as much scientific understanding as possible. Nutritional advice traditionally given to all pregnant women, including those with gestational diabetes mellitus (GDM) or noninsulin-dependent diabetes, does not allow for individual differences in caloric needs as a function of the degree of maternal obesity and thus, may encourage excessive weight gain. Evidence reviewed below suggests that adjusting caloric intake to meet new guidelines for weight gain during pregnancy may be advantageous in reducing maternal blood sugar and insulin levels, without producing abnormalities in other metabolic variables. Modest caloric reduction which limits excessive weight gain in the mother may also be associated with a small reduction of fetal weight. However, more stringent dietary manipulations in obese gravida should be discouraged as a routine measure until more knowledge is available from large-scale clinical trials about their effects on the entire panoply of maternal nutrients and their impact on the offspring.

Body Weight↗
PubMed1995

Antiaging action of caloric restriction: endocrine and metabolic aspects.

Restricting the energy intake of mice and rats slows the rate of actuarial aging, delays or prevents most age-associated disease processes, and maintains physiological processes in a youthful state at advanced ages. This manipulation is effective when initiated in young animals or in adult life. Although body fat is decreased by this reduction in energy intake, the reduction in body fat is not causally related to the antiaging action. Nor does this reduction in energy intake slow the aging processes by decreasing the metabolic rate, but it may do so by altering the characteristics of fuel use. Another possible mechanism underlying the antiaging action is the general protection restriction of energy intake provides against harmful agents, an action which may be the result of an alteration in adrenal glucocorticoid physiology.

Adult↗
PubMed2001

Chaperone-mediated regulation of hepatic protein secretion by caloric restriction.

Calorie restriction (CR) delays age-related physiological changes, reduces cancer incidence, and increases maximum life span in mammals. Here we show that CR decreased the expression of many hepatic molecular chaperones and concomitantly increased the rate and efficiency of serum protein secretion. Hepatocytes from calorie-restricted mice secreted twice as much albumin, 63% more alpha1-antitrypsin, and 250% more of the 31.5-kDa protein 2 h after their synthesis. A number of trivial explanations for these results, such as differential rates of protein synthesis and cell leakage during the assay, were eliminated. These novel results suggest that CR may promote the secretion of serum proteins, thereby promoting serum protein turnover. This may reduce the circulating level of damaging, glycoxidated serum proteins.

Animals↗