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PubMed2006

Evidence for hypermetabolism in boys with constitutional delay of growth and maturation.

CONTEXT: Children with constitutional delay of growth and maturation (CDGM) tend to be thin and have a growth pattern reminiscent of nutritional insufficiency. OBJECTIVE: Our objective was to compare differences in nutrition, body composition, bone mineral density, and resting and total energy expenditure (REE/TEE) in boys with CDGM and controls. We hypothesized that an imbalance between energy intake and expenditure may contribute to the pathogenesis of CDGM. DESIGN AND SETTING: We conducted an observational, cross-sectional study at an outpatient clinical research center. PATIENTS: Patients included 36 boys (8-17 yr): 12 with CDGM (short stature, delayed bone age and puberty, and no other pathology) and 12 height-matched (pre- or early-pubertal) and 12 age-matched (pubertal) healthy controls. MAIN OUTCOME MEASURES: Outcome measures included doubly labeled water studies (TEE), serum nutritional/hormonal markers, dual-energy x-ray absorptiometry, dietary analysis, and indirect calorimetry (REE). RESULTS: Nutritional markers were comparable among the groups. CDGM subjects had bone mineral density lower than age-matched controls (P < 0.01) but comparable with height-matched controls. Even though REE did not differ between groups, CDGM subjects had 25% higher caloric intake adjusted for fat-free mass (FFM) than height-matched controls (P < 0.05) and 78% higher caloric intake per kilogram FFM compared with age-matched controls (P < 0.00001). CDGM subjects had 46% (P < 0.05) and 91% (P < 0.001) higher TEE per kilogram FFM than height- and age-matched controls, respectively. CDGM subjects had lower IGF-I and testosterone than age-matched controls (P < 0.001) but levels were comparable with height-matched controls. CONCLUSIONS: Boys with CDGM have higher rates of overall energy expenditure compared with age- and size-matched controls. This increased metabolism may result in impaired tempo of growth. Additional studies are needed to determine whether augmenting nutrition to match their energy needs (with or without hormonal therapy) can improve linear and ponderal growth in patients with CDGM.

Adolescent↗
PubMed1988

Factors that may effect the reduction of hunger and body weight following d-fenfluramine administration.

Three studies have been undertaken to investigate why there are individual differences in the response to d-fenfluramine with respect to food intake and hunger in the short term and on body weight loss in the long term. Fenfluramine and norfenfluramine plasma levels have been used as probes to help detect and normalize these variances. In a single dose ranging volunteer study (0, 30, 40, and 60 mg), d-fenfluramine levels were significantly related to caloric intake and hunger rating scales when compared individually, and the slopes of the regression lines showed intersubject variation. These slopes, an index of each subject's response to fenfluramine, appear to be related to both the percentage underweight and more weakly to the percentage overweight. Those subjects at the extremes of weight showed a greater response to a given drug level. In two placebo-controlled 3 month studies (30 mg/day), the variances in weight loss were not explained by steady state drug levels, the percentage overweight, initial weight, duration of obesity, or caloric intake even when weight loss was normalized for differences in drug levels. Age, however, was significantly related to weight loss, with each additional 10 years increasing weight loss by approximately 1 kg. If confirmed, the sensitivity of fenfluramine anorexia may be an objective acute test of the central control of food intake. However, in long term clinical studies, drug levels were only weakly related to weight loss and other undefined factors seem to determine which patients responded better to fenfluramine treatment.

Adult↗
PubMed2005

Weight loss associated with reduced intake of carbohydrate reduces the atherogenicity of LDL in premenopausal women.

The effect of a 3-tier intervention including dietary modifications (ie, moderate energy restriction, decreased carbohydrate, increased protein), increased physical activity, and the use of carnitine as a dietary supplement was evaluated on plasma lipids and the atherogenicity of low-density lipoprotein (LDL) particles in a population of overweight and obese premenopausal (aged 20-45 years) women. Carnitine or a placebo (cellulose) was randomly assigned to the participants using a double-blind design. Carnitine supplementation was postulated to enhance fat oxidation resulting in lower concentrations of plasma triglycerides. Seventy women completed the 10-week protocol, which followed a reduction in their energy intake by 15% and a macronutrient energy distribution of 30% protein, 30% fat, and 40% carbohydrate. In addition, subjects increased the number of steps taken per day by 4500. As no differences were observed between the carnitine and placebo groups in all the measured parameters, all subjects were pooled together for statistical analysis. Participants decreased (P<.01) their caloric intake (between 4132.8 and 7770 kJ) and followed prescribed dietary modifications as assessed by dietary records. The average number of steps increased from 8950+/-3432 to 12764+/-4642 (P<.001). Body weight, plasma total cholesterol, LDL cholesterol, and triglyceride were decreased by 4.5%, 8.0%, 12.3%, and 19.2% (P<.0001), respectively, after the intervention. Likewise, apolipoproteins B and E decreased by 4.5% and 15% (P<.05) after 10 weeks. The LDL mean particle size was increased from 26.74 to 26.86 nm (P<.01), and the percent of the smaller LDL subfraction (P<.05) was decreased by 26.5% (P<.05) after 10 weeks. In addition, LDL lag time increased by 9.3% (P<.01), and LDL conjugated diene formation decreased by 23% (P<.01), indicating that the susceptibility of LDL to oxidation was decreased after the intervention. This study suggests that moderate weight loss (<5% of body weight) associated with reduced caloric intake, lower dietary carbohydrate, and increased physical activity impacts the atherogenicity of LDL.

Adult↗
PubMed1992

Economic analysis of the effects of caloric alternatives and reinforcer magnitude on "demand" for food in baboons.

In a study examining "demand" for food, the responses of six adult male baboons (Papio c. anubis) were maintained under a fixed ratio schedule of food reinforcement during daily 22-h experimental sessions. Completion of the ratio requirement resulted in the delivery of a single 1-g food pellet. Caloric intake was studied under four food-access conditions: a single source of 1-g food pellets, two sources of pellets with different response costs, one source of pellets and one source of dextrose solutions with different response costs, or a single source of multiple pellets. Total daily caloric intake under minimal response-cost conditions did not vary across these four conditions. Increasing the response requirement for a single pellet decreased daily food intake. Compared to this single-pellet condition, increasing the response requirement: (a) decreased intake of multiple pellets to a much smaller extent; (b) decreased pellet intake to a larger extent when dextrose was available on an alternate lever and (c) decreased pellet intake to the greatest extent when pellets were available on an alternate lever. Changes in pellet intake were fitted to a theoretical equation derived by Hursh et al. (1988) to describe changes in demand for a commodity. Increasing the number of pellets per delivery decreased the rate of change in intake as cost increased, indicating decreased elasticity. Dextrose availability increased the rate of change in intake as cost increased, indicating increased elasticity. Availability of an identical food source increased the initial slope of intake without effecting the rate of change, thus also increasing elasticity. Mathematical analysis of demand curves provide a means of comparing the effects of diverse environmental manipulations on feeding behavior.

Animals↗
PubMedDate not supplied

Nutritional alterations and the effect of fish oil supplementation in dogs with heart failure.

Alterations in body composition and nutritional status are common in humans with heart failure and are related, in part, to increases in cytokine concentrations. Cytokines have not been studied previously in dogs with naturally occurring cardiac disease nor has fish oil administration been used in this population to decrease cytokine production. The purposes of this study were to characterize nutritional and cytokine alterations in dogs with heart failure and to test the ability of fish oil to reduce cytokines and improve clinical outcome. Body composition, insulinlike growth factor-1, fatty acids, and cytokines were measured in 28 dogs with heart failure and in 5 healthy controls. Dogs with heart failure then were randomized to receive either fish oil or placebo for 8 weeks. All parameters were measured again at the end of the study period. At baseline, 54% of dogs with heart failure were cachectic and the severity of cachexia correlated with circulating tumor necrosis factor-alpha concentrations (P = .05). Cytokine concentrations at baseline, however, were not significantly increased in dogs with heart failure compared to controls. Baseline plasma arachidonic acid (P = .02), eicosapentaenoic acid (P = .03), and docosahexaenoic acid (P = .004) concentrations were lower in dogs with heart failure than in controls. Fish oil supplementation decreased interleukin-1 beta (IL-1) concentrations (P = .02) and improved cachexia (P = .01) compared to the placebo group. The mean caloric intake of the heart failure dogs as a group was below the maintenance energy requirement (P < .001), but no difference was found in food intake between the fish oil and placebo groups. Insulinlike growth factor-1 concentrations (P = .01) and reductions in circulating IL-1 concentrations over the study period (P = .02) correlated with survival. These data demonstrate that canine heart failure is associated with cachexia, alterations in fatty acids, and reduced caloric intake. Fish oil supplementation decreased IL-1 concentrations and improved cachexia. In addition, reductions in IL-1 predicted survival, suggesting that anticytokine strategies may benefit patients with heart failure.

Animals↗
PubMed1990

Nutritional assessment and support in chronic obstructive pulmonary disease.

Malnourished COPD patients demonstrate energy requirements significantly above predicted needs especially during activity. Recognition of this altered metabolic state is essential to the design of any nutritional intervention program. This factor alone, however, cannot explain the wasting syndrome observed in these patients. The elevated demands appear to combine with recognized factors which act to limit caloric intake. Nutritional repletion with calorie and protein supply proportional to demand is associated with weight gain, nitrogen retention, and improvement in physiologic parameters of muscle strength. Greater success of outpatient nutritional repletion in this population is dependent on alternative feeding strategies to deal with those symptoms which limit caloric intake, especially during a disease exacerbation. Future clinical research must explore these strategies before an adequate assessment of the risk and cost-benefit ratio of nutritional intervention can be determined. Additional work is indicated in techniques to identify those patients who would benefit from calorie supplementation as well as techniques to monitor the response of these individuals. Information gathered from the continued study of this population of stable outpatients with COPD will have wide application to the entire COPD patient population. This includes those patients with respiratory failure on mechanical ventilation, where numerous complicating factors makes the study of nutritional intervention and respiratory muscle function difficult.

Body Constitution↗
PubMedDate not supplied

Effects of chronic ethanol consumption on male Syrian hamster hepatic, microsomal mixed-function oxidases.

Chronic alcohol consumption significantly increases the risk of drug interactions. We have described its effects on hamster microsomal monooxygenases. Male Syrian hamsters (85 g) were given 10% ethanol in water and food ad lib for up to 6 weeks. Microsomal electron transport components and metabolism of ethylmorphine, benzphetamine, aniline, and acetaminophen were measured. At 4 weeks, SDS-PAGE of ethanol microsomes showed an induced band with an Mr of 53,900 daltons and there was a 2-3 fold stimulation of aniline and acetaminophen metabolism. Cytochrome P-450 increase was not significant. For the six week period, Caloric intake (3 weeks, p less than 0.001), liquid consumption (3 weeks, p less than 0.05) and body weights (6 weeks, p less than 0.05) of ethanol animals were significantly greater than controls; kidney weights were significantly less (p less than 0.05). Ethanol consumption increased from 20% of the daily caloric intake (week 1) to 31% (week 6). Induction of specific substrate metabolism without apparent deleterious physiological changes establishes hamsters fed 10% ethanol in drinking water as a biochemical model for the study of chronic alcohol consumption and specific drug interactions.

Animals↗
PubMed1998

Influence of dietary factors on actinically-induced skin cancer.

The first indication that high dietary fat intake could influence the development of ultraviolet (UV) radiation-induced skin cancer in experimental animals was reported in 1939. In the 1980s a series of animal studies showed that a high level of dietary fat intake markedly shortened the time between UV exposure and tumor appearance and increased the number of tumors that developed. Further, high levels of dietary fat affected skin cancer development at the promotional stage of UV-carcinogenesis, i.e., after the cancer causing dose of UV had been delivered. Perhaps more important, switching from a high-fat to a low-fat diet immediately after delivery of the UV-initiating dose negated the exacerbating effect of high fat intake. The latter finding suggested that dietary modification, even after a cancer-causing exposure to UV, might represent a potentially important intervention strategy in the prevention of non-melanoma skin cancer (NMSC) and provided the rationale for undertaking a dietary intervention trial. One hundred and fifteen skin cancer patients completed the 2-year clinical trial on the effect of a low-fat diet on occurrence of actinic keratosis (AK) and NMSC. Patients were randomly assigned to either continue their usual diet (control group, NI) or to adopt a diet with 20% of total caloric intake as fat (diet intervention group, DI). All patients were examined at 4-month intervals for new AK and NMSC. At baseline, the mean percent of caloric intake as fat was 40+/-4% in the NI group and 39+/-3% in the DI group. After 4 months of dietary therapy, the percent calories as fat had decreased to 21+/-7% in the DI group. The percent of calories as fat in the NI group did not drop below 37% during the study period. The cumulative number of new AK per patient from months 4 through 24 was 11.6+/-17 in the NI group and 3.2+/-6 in the DI group (P < 0.001). Numbers of new NMSC were analyzed in 8-month periods. There were no significant changes in NMSC occurrence in the NI group. However, NMSC occurrence in the DI group declined significantly (P < 0.02) in the last 8-month period. Patients in the DI group also had significantly (P < 0.01) fewer NMSC in the last 8-month period than did patients in the NI group (0.02 versus 0.26). Practical dietary advice, with respect to reduction of percent of calories as fat, could make an important contribution to the prevention and management of AK and NMSC.

Animals↗
PubMed1985

Manganese deficiency: effects on susceptibility to ethanol toxicity in rats.

Previous studies have shown that manganese (Mn) deficiency in rats results in reduced activity of manganese superoxide dismutase (MnSOD) and increased levels of mitochondrial lipid peroxidation. These findings suggested to us that the Mn-deficient rat may be especially susceptible to the toxic effects of ethanol, as the metabolism of this compound results in production of superoxide anion. Offspring from Mn-sufficient and Mn-deficient adult rats were given either 20% (wt/vol) ethanol or distilled-deionized water as their drinking fluid for 14 d. Response to ethanol feeding was different between Mn-sufficient and deficient rats as evidenced by severe reductions in caloric intake and body weight observed in the Mn-deficient rats. Furthermore, after 14 d of ethanol feeding, these rats were extremely lethargic and in poor physical condition. Although Mn-sufficient rats responded similarly to the deficient rats during the first 6 d of ethanol feeding, they increased their caloric intake and body weight during the remainder of the experimental period. MnSOD activity in the ethanol-fed Mn-sufficient and Mn-deficient rats was similar, thus the alcohol-induced toxicity observed in the deficient rats was not due to reduced MnSOD activity. Iron-induced lipid peroxidation may be one of the mechanisms leading to the toxicity observed, as ethanol feeding resulted in liver Fe levels that were 30% higher than those in Mn-deficient rats that were not fed ethanol.

Animals↗
PubMed2002

An assessment of obesity among African-American women in an inner city primary care clinic.

Despite multiple patient assessments and interventions, obesity continues to cause significant morbidity and mortality nationwide. This study assesses the prevalence of obesity and weight control practices among middle-aged African-American women. In 1995, 307 women 30 years of age and older were consecutively selected in a non-random fashion from three clinic sites located within a public university hospital that served largely indigent, inner city African-American populations. Interviewers surveyed the respondents using the Centers for Disease Control and Prevention's Behavioral Risk Factor Surveillance System (BRFSS). The prevailing demographic profile of patients in the clinic was middle-aged, indigent, ill, and of low educational attainment. Over 35% of individuals were classified as being overweight (BMI 25 to 29.9 kg/m2) and 45% were classified as being obese (BMI > or = 30 kg/m2). Therefore, more than 80% of individuals in this study were either overweight or obese, with BMI exceeding 25 kg/m2. Of the overweight and obese African-American women in this study, only 40% were attempting current weight loss practices, and weight loss attempts varied directly with body mass index. Although 80% of women attempted weight loss by restricting caloric intake, only 50% were also using physical activity as part of their regime. African-American women in this population have a higher prevalence of obesity and encounter great difficulty losing weight. Counselors should emphasize the value and ease of adopting a moderate regimen of physical activity and not just reducing caloric intake when advising African-American women and their peer network.

Adult↗
PubMed1978

Treatment of alcoholic hepatitis with encephalopathy. Comparison of prednisolone with caloric supplements.

A previous report from this institution demonstrated significant improvement of caloric intake and survival in patients with alcoholic hepatitis and hepatic encephalopathy given prednisolone when compared with placebo. The purpose of this study was to compare the effects of prednisolone with a regimen of 1600 calories per day without prednisolone. Fourteen patients with alcoholic hepatitis and encephalopathy were studied. All 7 on caloric supplementation and 2 of 7 given prednisolone died (p less than 0.01). These results suggest that prednisolone therapy reduces the mortality of those patients with alcoholic hepatitis and hepatic encephalopathy. This effect does not appear to be related to total caloric intake.

Adult↗
PubMedDate not supplied

[Bioelectric impedance in the nutritional evaluation of mentally deficient quadriplegic adults].

Severely mentally retarded persons with cerebral palsy show a high rate of acute and chronic malnutrition. Without discarging other factors which might be at play, caloric intake deficiency stemming from the difficulties involved in being fed appear to play a crucial role in its etiology. In the assessment of these disorders, anthropometry is limited by the lack of adequate reference values and by the difficulty or impossibility of measuring height using the conventional method. The purpose of this study is to see how changes in body composition brought about by an increase in dietary caloric intake are perceived by both anthropometry and biolectrical impedance analysis. To do so, 13 subjects were selected from a group of 203 severely mentally retarded persons made up of 25% cerebral palsy patients and 13% quadriplegics. The 13 subjects were fed orally without tubes and all had tricipital skinfolds of less than P25. All 13 were given a 25% caloric increase over the regular diets for a period of two months. This increase was provided by means of a polymeric, normoproteic, hypercaloric preparation. Weight and brachial perimeter showed significant increases coinciding with the administration of the supplement. Theses increases were not noticeable two months after discontinuing the supplement. There were no significant changes in tricipital and subescapular skinfolds, muscular circumference of de mid-arm, resistance, reactance, or the total body an extracellular water calculated from the latter two values. From these results we deduce that biolectrical impedance analisys offers no advantages over anthropometry in monitoring the nutritional status of quadriplegics.

Adult↗
PubMedDate not supplied

Comparison of the acute and long-term effects of exercise on glucose control in type I diabetes.

To determine the long-term effect of exercise training on glucose control, 13 subjects with type I diabetes and 7 control subjects performed 45 min of cycle exercise three times per wk for 12 wk. The acute blood glucose response, the long-term effect on glucose control (glycosylated hemoglobin and fasting plasma glucose), and changes in nutrient intake were assessed. Fitness as measured by VO2 MAX increased in both control (33.8 +/- 1.7 to 43.2 +/- 3.5 ml/min/kg) and diabetic (38.7 +/- 3.3 to 46.5 +/- 3.6 ml/min/kg) (P less than 0.05) subjects although body weight remained unchanged. In the diabetic subjects, an acute glucose-lowering effect occurred with each exercise session throughout the 12-wk training period (225.8 +/- 16.1 to 148.5 +/- 16.8 mg/dl, P less than 0.001). However, fasting plasma glucose and glycosylated hemoglobin remained essentially unchanged (pretraining, 193.7 +/- 27.5 mg/dl and 10.7 +/- 0.3%; 6-wk training, 192.5 +/- 27.1 mg/dl and 10.7 +/- 0.03%; 12-wk training, 202 +/- 30.1 mg/dl and 10.3 +/- 0.8%). Total caloric intake as assessed by diet history increased significantly on exercising days (2569-2849 kcal, P less than 0.05). Although plasma glucose decreases acutely with exercise, increased caloric intake on exercising days obviates a long-term effect of training on glucose control. More precise guidelines and recommendations as to exercise timing and nutrient intake, likely based on self-monitoring of blood glucose, are required to achieve a beneficial effect of exercise training on metabolic control in type I diabetes.

Adult↗
PubMed1991

Nutrition and the use of metabolic assessment in the ventilator-dependent patient.

Nutritional support is an important aspect of care in hospitalized patients, especially those receiving mechanical ventilation. While nutritional assessments can help guide the clinician in determining appropriate caloric intake requirements and refeeding schedules, few tools exist to evaluate the consequences of over- or underfeeding. Metabolic assessment using indirect calorimetry is a new method of nutritional assessment for use at the bedside of the weaning patient. The data obtained from a metabolic assessment can be used to adjust formulas and total caloric intake as well as differentiate between dead space and elevated carbon dioxide production as reasons for persistent hypercarbia.

Calorimetry, Indirect↗
PubMed2003

Current biochemical studies of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis suggest a new therapeutic approach.

The study population in this report by Lin et al. was ob/ob mice that have an inherited genetic deficiency of the appetite-suppressing hormone leptin. These mice develop hyperinsulinemia, insulin resistance, and fatty livers. Compared with their lean littermates and wild-type C57BL-6 mice, ob/ob mice have hepatomegaly. In this study, the authors compared three different groups of adult mice (aged 8-10 wk), including male ob/ob C57BL-6 mice, their lean littermates, and wild-type C57BL-6 mice of the same age and sex. The primary purpose of this study was to test the efficacy of metformin for treatment of fatty liver disease in obese, ob/ob mice that develop hyperinsulinemia or insulin resistance and fatty livers. Metformin therapy was found to eliminate fatty liver disease in this model. The potential mechanisms of the action of metformin were the inhibition of hepatic tumor necrosis factor (TNF)alpha and several TNF-inducible responses, which are likely to promote hepatic steatosis and necrosis. In these experiments, ob/ob mice were divided into three treatment groups. Group 1 consisted of eight mice that were treated with metformin and permitted to consume a nutritiously replete liquid mouse diet ad libitum. Mice in group 2 (n = 8) did not receive metformin but were pair-fed the same volume of liquid diet that the mice in the metformin-treated group had consumed on the previous day. Obese ob/ob mice in group 3 (n = 4) and lean mice received no metformin, as with the mice in group 2, but were permitted to consume the liquid diet ad libitum. Liquid diet was given to facilitate accurate daily comparison of food intake among the various treatment groups. All mice were weighed at the beginning of the study and weekly thereafter until killed and then sera, fat, and liver tissues were collected. Tissues were either fixed in buffered formalin and processed from the deceased mice for histology or snap frozen in liquid nitrogen and stored until RNA and proteins were isolated. The feeding protocol was repeated with a second group of 18 ob/ob mice. After 4 wk, hepatocytes were obtained by in situ liver perfusion with collagenase and assayed for cellular adenosine triphosphate (ATP) content. In each experiment, hepatocytes isolated from 3 mice from each treatment group were suspended in a medium and pooled for subsequent analysis to evaluate cell viability, determine the number of obtained cells, and to assay cellular ATP content. These experiments were repeated using another 3 mice from each treatment group, so that analysis of hepatocytes took place from six ob/ob mice in each feeding group.Hepatic steatosis was decreased significantly only in the metformin-treated group. The authors found that metformin's beneficial effect on the fatty liver disease of mice was not due to its ability to constrain hyperphagia, nor due to decreased caloric ingestion, because the daily caloric intakes of the metformin-treated mice and the pair-fed control mice were virtually identical. These caloric intakes were consistently approximately 20% less than that of another obese control group that was permitted to consume diet ad libitum. The authors also observed no significant effect of metformin on serum glucose concentration from fed, ob/ob mice. Metformin is known to reduce hyperinsulinemia by about 40% in both of these obese hyperinsulinemic and insulin-resistant rodent strains. In conclusion, Lin et al. documented that metformin improves fatty liver disease and reverses hepatomegaly, steatosis, and aminotransferase abnormalities in mice. In addition, the authors suggest that metformin might inhibit dieting-induced redistribution of lipid from the liver to adipose tissue depots. In summary, this study identifies a potential treatment for fatty liver disease in humans.

Adult↗
PubMed2000

The effect of dehydroepiandrosterone on Zucker rats selected for fat food preference.

When allowed to select between macronutrients in a 1-h-a-day meal paradigm, Zucker rats consume 20-80% of their total caloric intake as fat. If they receive an intraperitoneal injection of DHEA 2 h before such a test meal, they consume fewer total calories. The magnitude of this effect on each macronutrient depends upon the animal's initial preference for fat; the higher the initial fat preference, the more profound is the decrease in caloric intake and the more pronounced the effect on fat consumption. Doses as low as 25 mg DHEA/kg body weight are effective. Lean Zucker rats that prefer to consume a high-fat diet have higher epinephrine and dopamine levels in select regions of the hypothalamus known to control food intake. Administration of DHEA to such animals 2 h before decapitation reduces the content of norepinephrine and these monoamines to levels that mimic the values found in the low-fat-preferring animals. It is hypothesized that exogenous DHEA causes the acute release of norepinephrine, epinephrine, and dopamine in select regions of the hypothalamus, and this release causes a decrease in food intake, particularly fat.

Animals↗
PubMed2002

The effects of high-fat diet on exercise-induced changes in metabolic parameters in Zucker fa/fa rats.

The objectives of this study were to document the effects of moderate aerobic exercise on insulin secretion and other metabolic indices in fa/fa rats and to determine if a high-fat (HF) diet altered these effects. Six-week-old fa/fa and lean Zucker rats were either sedentary or exercised by daily swimming for 4 weeks. Half of the exercised and sedentary rats were fed a diet with 16% fat and 44% carbohydrate, while the control groups were fed a diet with 4.5% fat and 49% carbohydrate. At the end of 4 weeks, caloric intake, weight gain, plasma hormone and nutrient levels, and oral glucose tolerance were measured. The pancreatic islet beta-cell function was assessed by measuring glucose-stimulated insulin secretion, glucose phosphorylating activity, and free fatty acid (FFA) oxidation in cultured islets. In fa/fa rats fed the control diet, exercise reduced weight gain, caloric intake, and fasting plasma triglyceride (TG) concentrations without affecting fasting glucose and insulin concentrations. HF diet blocked the effects of exercise on weight gain and food intake and worsened insulin resistance of fa/fa rats. In vitro, neither exercise nor HF diet alone affected islet beta-cell function. However, in combination, exercise and high dietary fat reduced glucokinase sensitivity to glucose and increased islet cell response to mannoheptulose inhibitory actions. We conclude that beneficial effects of moderate exercise on metabolism are not mediated by effects on pancreatic beta cells. Diets elevated in fat decrease the beneficial effects of exercise on metabolic indices in vivo.

Animals↗
PubMed1993

Modulation of oxidative DNA damage levels by dietary fat and calories.

Decreased dietary intake of fat and/or calories generally results in a lower incidence of mammary gland tumors in rodents. Feeding of either low-fat or calorie-restricted diets to rats also has been shown to result in decreased levels of oxidative DNA damage. Since oxidative DNA damage is suggested to have a role in carcinogenesis, this may be one mechanism by which dietary change can reduce cancer risk. The effects of calorie-restricted diets on both oxidative DNA damage levels and mammary gland tumor incidence are generally more pronounced than that of low-fat diets. There is, however, some difficulty in defining what amount of fat should be used to prepare 'low-fat' and 'high-fat' rodent diets as well as what a suitable fat intake for control diets should be in studies that examine the effects of dietary fat and/or calories on tumorigenesis. In particular, the promoting effects of dietary fat may be exerted only up to a certain level of fat, above which no further effect is observed. Another difficulty in the interpretation of the results is that there may be a time-dependent effect of high fat diets on oxidative damage, with increased damage resulting only when the diets are fed for longer periods of time. The appropriate experimental approach to model human dietary exposures therefore remains to be determined. Although the effects of caloric intake on mammary gland tumorigenesis appear to be more pronounced than that of fat intake, low-fat diets still may be useful as a preventive measure in human populations to reduce breast cancer risk for individuals who cannot safely reduce their caloric intake.

Animals↗