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At least 919 records · Page 51Linked to original sources
PubMed2002

Role of sibutramine in the treatment of obese Type 2 diabetic patients receiving sulphonylurea therapy.

AIMS: To investigate whether the satiety-inducing agent sibutramine affected body weight and associated anthropometry in overweight and obese (body mass index (BMI) > 27) Type 2 diabetic patients on sulphonylurea therapy. METHODS: A randomized, placebo-controlled trial was undertaken in 134 patients with stable metabolic control on chronic sulphonylurea therapy. Patients were placed on moderate caloric restriction and received treatment with either sibutramine (15 mg/day) or placebo for 6 months. RESULTS: Fifty-three of 69 sibutramine-treated and 57/65 placebo-treated patients completed the study. Both groups showed progressive weight loss. At the end of the trial weight loss was two times greater in the sibutramine group (mean +/- SEM; -4.5 +/- 0.5 kg) than placebo (-1.7 plus minus 0.5 kg, P < 0.001 vs. sibutramine). There was a trend for more patients to lose > 5% of initial body weight in the sibutramine group than placebo. BMI (P < 0.001) and waist circumference (P < 0.001) were also decreased to a greater extent by sibutramine. Mean reductions in HbA(1c) were commensurate with weight loss in both the sibutramine and placebo (- 0.78 +/- 0.17% and -0.73 +/- 0.23%; P = 0.84). Sibutramine was well tolerated with only two patients withdrawn due to potentially drug-related serious adverse events (palpitations). CONCLUSIONS: Sibutramine, in conjunction with moderate caloric restriction, enhances weight loss and reduces waist circumference in overweight and obese Type 2 diabetic patients receiving sulphonylurea therapy. This is associated with additional improvements in glycaemic control in a limited number of patients losing > or = 10% of their baseline body weight.

Appetite Depressants↗
PubMed2003

Mechanisms of dairy modulation of adiposity.

Dietary calcium plays a pivotal role in the regulation of energy metabolism, in that we have found high calcium diets to attenuate adipocyte lipid accretion and weight gain during periods of overconsumption of an energy-dense diet and to increase lipolysis and preserve thermogenesis during caloric restriction, thereby markedly accelerating weight loss. Our studies of the agouti gene in obesity and insulin resistance demonstrate a key role for intracellular Ca(2+) in regulating adipocyte lipid metabolism and triglyceride storage, with increased intracellular Ca(2+), resulting in stimulation of lipogenic gene expression and lipogenesis, and suppression of lipolysis, resulting in adipocyte lipid filling and increased adiposity. Moreover, we have recently demonstrated that the increased calcitriol produced in response to low calcium diets stimulates Ca(2+) influx in human adipocytes and thereby promotes adiposity. Accordingly, suppressing calcitriol levels by increasing dietary calcium is an attractive target for the prevention and management of obesity. In support of this concept, transgenic mice expressing the agouti gene specifically in adipocytes (a humanlike pattern) respond to low calcium diets with accelerated weight gain and fat accretion, whereas high calcium diets markedly inhibit lipogenesis, accelerate lipolysis, increase thermogenesis and suppress fat accretion and weight gain in animals maintained at identical caloric intakes. Further, low calcium diets impede body fat loss, whereas high calcium diets markedly accelerate fat loss in transgenic mice subjected to caloric restriction. Notably, dairy sources of calcium exert markedly greater effects in attenuating weight and fat gain and accelerating fat loss. This augmented effect of dairy vs. supplemental calcium is likely attributable to additional bioactive compounds in dairy that act synergistically with calcium to attenuate adiposity; among these are angiotensin converting enzyme inhibitory peptides, which limit angiotensin II production and thereby limit angiotensin II stimulation of adipocyte lipogenesis. These concepts are confirmed by both epidemiological and clinical data, which similarly demonstrate that dairy products exert a substantially greater effect on both fat loss and fat distribution compared to an equivalent amount of supplemental calcium.

Adipocytes↗
PubMed2000

Slow recovery of body fat lost during adenovirus-induced hyperleptinemia.

In normal rats, adenovirus-induced hyperleptinemia causes disappearance of visible body fat, downregulation of lipogenic enzymes, and upregulation of oxidative enzymes and thermogenic proteins. In addition, preadipocyte markers replace mature adipocyte markers, suggesting dedifferentiation. In weight loss induced by caloric restriction, by contrast, the lipogenic machinery is essentially intact. To determine if the radical changes induced by leptin would slow the reappearance of body fat, we compared normal lean rats made hyperleptinemic by infusing an adenovirus-leptin construct with diet-matched littermates. Initially, in plasma leptin the hyperleptinemic rats averaged approximately 50x the controls and, although it declined progressively, it was still slightly elevated at 150 days (P < 0.05). In the hyperleptinemics, body fat mass, quantified by magnetic resonance spectroscopy, remained below the pretreatment value for 60 days, while in diet-matched controls it exceeded the pretreatment value. Epididymal fat pad weight in hyperleptinemics was still 28% below paired controls at 150 days posttreatment. Histologic examination revealed adipocytes of hyperleptinemic animals to be smaller 60 days after treatment. At 60 days, adipose tissue UCP-2 gene expression in hyperleptinemics was still above controls, but expression of other lipogenic and oxidative enzymes had returned to baseline expression levels. We conclude that in normal rats recovery of body fat following adenovirus-induced hyperleptinemia is much slower than after caloric restriction, possibly because of persistent upregulation of adipocyte UCP-2.

Adenoviridae↗
PubMed1987

Dietary zinc deficiency increases the methylbenzylnitrosamine-induced formation of O6-methylguanine in the esophageal DNA of the rat.

Dietary zinc deficiency in combination with environmental exposure to methylbenzylnitrosamine (MBN) is associated with an increased incidence of esophageal carcinoma in man. The proposed mechanism of MBN-induced esophageal carcinoma is through metabolic activation of MBN to form benzaldehyde, and a carbonium ion which methylates DNA. MBN is known to methylate DNA forming O6-methylguanine (O6-MeG) adducts. These adducts can induce guanine to adenine point mutations and such mutations are responsible for certain carcinogen-induced tumors. Rats maintained on a zinc-deficient diet exhibit an increased incidence of MBN-induced esophageal carcinoma when compared with ad libitum and pair-fed controls. The caloric restriction of the pair-fed controls was associated with a lower incidence of MBN-induced esophageal carcinoma than was observed in the ad libitum controls. These differences in tumor incidence were associated with alterations in the formation and clearance of MBN-induced esophageal O6-MeG. Weanling male Sprague-Dawley rats were raised on egg protein diets containing 2.3 p.p.m. zinc (low zinc) or 50 p.p.m. zinc (control). One group of control animals was fed the control diet ad libitum and a second group pair-fed the control diet to match the intake of the zinc-deficient group. After 3 weeks on the diets the animals were injected with a single dose of MBN (2.0 mg/kg b.w.) and levels of esophageal O6-MeG were determined after 1, 3, 6 and 24 h. O6-MeG was significantly higher in the zinc-deficient animals than in controls, with the pair-fed controls demonstrating O6-MeG levels lower than the ad libitum controls. Thus, dietary zinc deficiency results in significantly increased levels of MBN-induced esophageal O6-MeG, and caloric restriction results in decreased levels of MBN-induced esophageal O6-MeG. These changes in esophageal O6-MeG may in part explain the increased incidence of MBN-induced esophageal carcinoma observed with dietary zinc deficiency.

Animals↗
PubMed1988

Effects of aerobic exercise on energy expenditure and nitrogen balance during very low calorie dieting.

Aerobic exercise in addition to severe caloric restriction was studied for its effects on resting energy expenditure (REE), weight loss, and lean tissue preservation in adult women. A formula diet providing 1.5 g protein and 0.5 g carbohydrate (CHO) per kilogram of ideal body weight daily (mean intake 720 kcal/d) was given to 12 overweight inpatients for 4 to 5 weeks. Six subjects remained sedentary (group 1), while the other six subjects (group 2) performed supervised endurance exercise (a total of 27 hours at 50% of maximal oxygen uptake (VO2max) over 4 weeks). Lean tissue preservation was excellent in both groups and was unaffected by the group 2 exercise regimen. Weight loss over 4 weeks in the two groups did not differ (group 1, 6.9 +/- 0.7 kg; group 2, 6.5 +/- 0.7 kg). The VO2max was not increased after 4 weeks of exercise compared with controls. The resting oxygen consumption (rVO2) of both groups declined 10% (P less than .001) in the first seven days of dieting. Thereafter the rVO2 in group 1 remained stable, but a further 17% reduction occurred in group 2 (P less than .03) by the third week of exercise. The free triiodothyronine (fT3) concentration also fell more in group 2 (P less than .05), suggesting a relationship between fT3 and energy expenditure during severe caloric restriction. The ergometer exercise for up to two hours daily was well tolerated. The absence of either a training effect or accelerated weight loss in group 2 may be due to the limited duration (4 weeks) or intensity of the exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed2001

Enhanced gluconeogenesis and increased energy storage as hallmarks of aging in Saccharomyces cerevisiae.

A relationship between life span and cellular glucose metabolism has been inferred from genetic manipulations and caloric restriction of model organisms. In this report, we have used the Snf1p glucose-sensing pathway of Saccharomyces cerevisiae to explore the genetic and biochemical linkages between glucose metabolism and aging. Snf1p is a serine/threonine kinase that regulates cellular responses to glucose deprivation. Loss of Snf4p, an activator of Snf1p, extends generational life span whereas loss of Sip2p, a presumed repressor of the kinase, causes an accelerated aging phenotype. An annotated data base of global age-associated changes in gene expression in isogenic wild-type, sip2Delta, and snf4Delta strains was generated from DNA microarray studies. The transcriptional responses suggested that gluconeogenesis and glucose storage increase as wild-type cells age, that this metabolic evolution is exaggerated in rapidly aging sip2Delta cells, and that it is attenuated in longer-lived snf4Delta cells. To test this hypothesis directly, we applied microanalytic biochemical methods to generation-matched cells from each strain and measured the activities of enzymes and concentrations of metabolites in the gluconeogenic, glycolytic, and glyoxylate pathways, as well as glycogen, ATP, and NAD(+). The sensitivity of the assays allowed comprehensive biochemical profiling to be performed using aliquots of the same cell populations employed for the transcriptional profiling. The results provided additional evidence that aging in S. cerevisiae is associated with a shift away from glycolysis and toward gluconeogenesis and energy storage. They also disclosed that this shift is forestalled by two manipulations that extend life span, caloric restriction and genetic attenuation of the normal age-associated increase in Snf1p activity. Together, these findings indicate that Snf1p activation is not only a marker of aging but also a candidate mediator, because a shift toward energy storage over expenditure could impact myriad aspects of cellular maintenance and repair.

Culture Media↗
PubMed2004

Ghrelin regulates mitochondrial-lipid metabolism gene expression and tissue fat distribution in liver and skeletal muscle.

Ghrelin is a gastric hormone increased during caloric restriction and fat depletion. A role of ghrelin in the regulation of lipid and energy metabolism is suggested by fat gain independent of changes in food intake during exogenous ghrelin administration in rodents. We investigated the potential effects of peripheral ghrelin administration (two times daily 200-micrograms [DOSAGE ERROR CORRECTED] sc injection for 4 days) on triglyceride content and mitochondrial and lipid metabolism gene expression in rat liver and muscles. Compared with vehicle, ghrelin increased body weight but not food intake and circulating insulin. In liver, ghrelin induced a lipogenic and glucogenic pattern of gene expression and increased triglyceride content while reducing activated (phosphorylated) stimulator of fatty acid oxidation, AMP-activated protein kinase (AMPK, all P < 0.05), with unchanged mitochondrial oxidative enzyme activities. In contrast, triglyceride content was reduced (P < 0.05) after ghrelin administration in mixed (gastrocnemius) and unchanged in oxidative (soleus) muscle. In mixed muscle, ghrelin increased (P < 0.05) mitochondrial oxidative enzyme activities independent of changes in expression of fat metabolism genes and phosphorylated AMPK. Expression of peroxisome proliferator-activated receptor-gamma, the activation of which reduces muscle fat content, was selectively increased in mixed muscle where it paralleled changes in oxidative capacities (P < 0.05). Thus ghrelin induces tissue-specific changes in mitochondrial and lipid metabolism gene expression and favors triglyceride deposition in liver over skeletal muscle. These novel effects of ghrelin in the regulation of lean tissue fat distribution and metabolism could contribute to metabolic adaptation to caloric restriction and loss of body fat.

Adenylate Kinase↗
PubMed2004

Age-related decline in caloric intake and motivation for food in rhesus monkeys.

Human studies have documented age-related declines in caloric intake that are pronounced at advanced ages. We examined caloric intake from a longitudinal study of aging in 60 male and 60 female rhesus monkeys (Macaca mulatta) collected for up to 10 years. Monkeys were provided a standardized, nutritionally fortified diet during two daily meals, and intake was measured quarterly. About half of the monkeys were on a regimen of caloric restriction (CR) representing about a 30% reduction in caloric intake compared to controls (CON) of comparable age and body weight. CR was applied to determine if this nutritional intervention retards the rate of aging in monkeys similar to observations in other mammalian studies. Following reproductive maturity at 6 years of age, there was a consistent age-related decline in caloric intake in these monkeys. Although males had higher intake than females, and CON had higher intake compared to CR, the sex and diet differences converged at older ages (>20 years); thus, older CR monkeys were no longer consuming 30% less than the CON. When adjusted for body weight, an age-related decline in caloric intake was still evident; however, females had higher intake compared to males while CR monkeys still consumed less food, and again differences converged at older ages. Motivation for food was assessed in 65 of the monkeys following at least 8 years in their respective diet groups. Using an apparatus attached to the home cage, following an overnight fast, monkeys were trained to reach out of their cage to retrieve a biscuit of their diet by pushing open a clear plastic door on the apparatus. The door was then locked, and thus the biscuit was irretrievable. The time spent trying to retrieve the biscuit was recorded as a measure of motivation for food. We observed an age-related decline in this measure, but found no consistent differences in retrieval time between CR and CON groups of comparable age and time on diet. The results demonstrate an age-related decline in food intake and motivation for food in rhesus monkeys paralleling findings in humans; however, we found no evidence that monkeys on a long-term CR regimen were more motivated for food compared to CON. Examining the relationship of selected blood proteins to food intake following 7-11 years on the study, we found a negative correlation between globulin and intake among males and females after accounting for differences in age. In addition, a positive correlation was observed between leptin and intake in males.

Age Factors↗
PubMed1994

Metabolic Implications of Obesity, Weight Loss and Energy Expenditure following Gastric Restrictive Surgery.

This review examines the energetics and metabolic parameters which influence the effectiveness of gastric restrictive surgery in achieving weight loss in the clinically severely obese patient. Among the subjects discussed are the metabolic determinants and consequences of obesity, energy expenditure and its components, factors other than dietary restriction and weight loss which affect energy expenditure, and the metabolic risk factors for weight gain. The role of exercise is reviewed, including the effects of exercise on energy balance and the thermic effect of food. The value of combining exercise with diet restriction, the effect of caloric restriction on the capacity to exercise and the place of exercise in the obese diabetic are examined. Finally, the metabolic consequences of gastric restrictive surgery, the adaptive response to surgically-induced weight loss and nutritional recommendations following gastric restrictive surgery are reviewed.

Journal Article↗
PubMed1992

Cardiac effects of caloric restriction-mechanisms and potential hazards.

The heart is not spared from the catabolic effects of undernutrition, but is subject to the same degree of weight loss as skeletal muscle. Pumping performance, however, is not reduced in proportion to myocardial wasting and thus functional protection prevents failure of the hypotrophic heart. In animal experiments, no major qualitative changes in myocardial composition apart from reduced myosin ATPase activity have been found. This reduction in ATPase activity might be associated with down-regulation of thyroid hormones and the development of insulin resistance and serve as an energy saving adaptation. Increased cardiac sensitivity to adrenergic stimulation may also constitute a means to increase heart performance in situations with augmented circulatory demands. On the other hand, increased sensitivity and maximum response to adrenergic stimulation might render the heart more susceptible to arrhythmia, and thus explain sudden unexpected death following rapid weight loss.

Animals↗
PubMed2002

[Pathophysiology and genetics of obesity].

Obesity has become the most prevalent nutritional disorder in post-industrialised societies and it is associated with the development of severe and costly complications such as type 2 diabetes mellitus and coronary heart disease or cancer. A large proportion of the risk of obesity is determined by the genetic susceptibility of an individual, but environmental factors conducive for the disorder play an important role in its phenotypic expression. Several candidate genes emerged from studies in animal models of obesity, but human pathophysiology is likely to be more complex. Thus, most cases of human obesity probably result from subtle interactions of susceptibility genes with environmental factors favouring deposition of excess calories as fat. The recent surge of obesity may relate to past evolutionary pressure which favoured selection of mechanisms defending body-weight against caloric restriction rather than against caloric excess. Rapidly developing new techniques in quantitative genetics and growing information from functional genomics will help to understand the interaction of environmental factors with signalling networks that regulate energy metabolism. The role of previously unknown pathways in the aetiology of obesity will be uncovered. The typing of numerous genetic variants will become possible and allow individual risk assessment for obesity and/or its associated disorders. Thus, rational and individually tailored therapies may be developed to combat obesity and its associated disorders.

Adult↗
PubMed1980

Relationships of maternal weight gain, prepregnancy weight, and infant birthweight. Interaction of weight factors in pregnancy.

A study of the effects of restricted vs. unrestricted maternal caloric intakes upon infant birthweights was conducted in a large, middle-class, private obstetrical practice in Madison. Wis. Comparison of data relating to 602 pregnancies showed that increases in maternal weight gain accompanied significant and desirable increases in infant birthweight. Findings in this study support the statement of the Food and Nutrition Board that caloric restriction during pregnancy may be undesirable and probably is detrimental to the newborn.

Adult↗
PubMed2007

Calorie restriction in nonhuman primates: assessing effects on brain and behavioral aging.

Dietary caloric restriction (CR) is the only intervention repeatedly demonstrated to retard the onset and incidence of age-related diseases, maintain function, and extend both lifespan and health span in mammals, including brain and behavioral function. In 70 years of study, such beneficial effects have been demonstrated in rodents and lower animals. Recent results emerging from ongoing studies of CR in humans and nonhuman primates suggest that many of the same anti-disease and anti-aging benefits observed in rodent studies may be applicable to long-lived species. Results of studies in rhesus monkeys indicate that CR animals (30% less than controls) are healthier than fully-fed counterparts based on reduced incidence of various diseases, exhibit significantly better indices of predisposition to disease and may be aging at a slower rate based on analysis of selected indices of aging. The current review discusses approaches taken in studies of rhesus monkeys to analyze age-related changes in brain and behavioral function and the impact of CR on these changes. Approaches include analyses of gross and fine locomotor performance as well as brain imaging. In a related study it was observed that short-term CR (6 months) in adult rhesus monkeys can provide protection against a neurotoxic insult. Increasing interest in the CR paradigm will expand its role in demonstrating how nutrition can modulate the rate of aging and the mechanisms responsible for this modulation.

Aging↗
PubMed1971

Prenatal cerebral development: effect of restricted diet, reversal by growth hormone.

Caloric restriction of rats from day 10 to day 20 of pregnancy results in significant decreases in body weight, placental weight, cerebral weight, cerebral DNA, and cerebral protein of the offspring at birth. These decreases did not usually occur if mothers on the restricted diet were treated concomitantly with bovine growth hormone. If growth hormone did not cross the placenta, then, it is postulated, at least one effect of growth hormone was the mobilization of maternal nutrient reserves.

Animals↗
PubMed1990

Changes in overall plasma norepinephrine turnover and lymphomonocyte beta-adrenoceptor number during combined caloric and sodium restriction in normotensive obese subjects.

The aim of the study was to evaluate in eight normotensive obese patients the influence of low sodium intake (9 mEq/day) on the sympathetic activity modifications induced by caloric restriction (2511 kJ/day). As compared to the isocaloric salt balanced diet, 7 days of normosodic underfeeding induced a decrease in the overall norepinephrine turnover (clearance and appearance rate) and 24 hours urinary output, whereas the combined caloric and salt restriction significantly increased the norepinephrine appearance rate and even more the norepinephrine clearance but, on the other hand, decreased the beta-adrenergic receptor number on the lymphomonocyte surface, suggesting a reduced peripheral sensitivity to catecholamines. Therefore, the utility of the combined sodium and caloric restriction in the treatment of the normotensive obese patients remains still questionable.

Adolescent↗
PubMed1993

Body fat distribution, blood pressure and blood glucose in Egyptian obese women undergoing a weight control program.

In a sample of 92 obese healthy women, 35 of them were chosen to follow a weight control program comprising both caloric restriction and exercise for three months. They were matched for age and weight with the remaining 57 women who also served as a control group. The entire sample was further stratified according to age into two categories of 20-34 and 35-50 years. The caloric supply was restricted to about 1000 kcal/day, in addition to a 1-h session of mild exercise which was performed twice weekly; the subjects' energy expenditure was 2200 kcal/day. Only the mean values of the biceps, triceps, and supra-iliac skinfold measurements were significantly decreased (p < 0.05) in the younger trained dieters when compared to their counterpart sedentary controls. On the other hand, obvious group variations appeared between body fat distribution when related to body weight and to blood pressure. Blood glucose revealed normal levels in the whole sample. Mean values were numerically lower in the older trained dieters than their matched sedentary controls, while they were significantly lower (p < 0.05) in the younger trained dieters. Although blood pressure was in the normal range for all participants, a nonsignificant decrease was recorded for both age groups of the obese trained dieters upon completion of the program. The systolic blood pressure decreased by 5.4% and the diastolic by 6.7% regarding the younger age, while the decrease in the older age was 3.5% for the systolic and 4.8% for the diastolic blood pressure. It was concluded that, although the trained dieters were still obese, the caloric restriction was promoted synergistically by exercise, leading to a more harmonious fat distribution and to lower normal levels of blood pressure and blood glucose.

Adipose Tissue↗
PubMed1992

Long-term potentiation is lost in aged rats but preserved by calorie restriction.

Recordings of synaptic population responses, post-tetanic potentiation (PTP) and long-term potentiation (LTP) were made from area CA1 in hippocampal slices from ad libitum-fed rats at about 2 and 24 months of age, and also in animals at about 24 months of age that had been restricted to 60% of the caloric intake of control animals since weaning. Both PTP and LTP were greatly reduced in the old ad-lib animals. Calorically-restricted rats at about 24 months of age showed hippocampal responses with initial peak amplitudes more like those of 2-month controls than the ad-lib animals at 24 months. These observations suggest that calorie restriction preserves nervous-system functions, including indicators of plasticity such as LTP, which are otherwise lost in aging.

Aging↗