Creatine monohydrate supplementation on body weight and percent body fat

Seventeen active males (age 22.9 +/- 4.9 year) participated in a study to examine the effects of creatine monohydrate supplementation on total body weight (TBW), percent body fat, body water content, and caloric intake. The TBW was measured in kilograms, percent body fat by hydrostatic weighing, body water content via bioelectrical impedance, and caloric intake by daily food log. Subjects were paired and assigned to a creatine or placebo group with a double-blind research design. Supplementation was given for 4 weeks (30 g a day for the initial 2 weeks and 15 g a day for the final 2 weeks). Subjects reported 2 days a week for supervised strength training of the lower extremity. Significant increases before and after the study were found in TBW (90.42 +/- 14.74 to 92.12 +/- 15.19 kg) and body water content (53.77 +/- 1.75 to 57.15 +/- 2.01 L) for the creatine group (p = 0.05). No significant changes were found in percent body fat or daily caloric intake in the creatine group. No significant changes were noted for the placebo group. These findings support previous research that creatine supplementation increases TBW. Mean percent body fat and caloric intake was not affected by creatine supplementation. Therefore weight gain in lieu of creatine supplementation may in part be due to water retention.     

Predictors of Weight Loss in Adults with Topiramate‐Treated Epilepsy

Objective: We examined predictors of weight loss with topiramate, an anticonvulsant associated with weight loss in adults. Research Methods and Procedures: In this uncontrolled, prospective clinical trial, topiramate was added to existing anticonvulsants in adults (40 to 110 kg) with partial‐onset seizures. Primary measurements were change from baseline weight after 3 months and 1 year in patients completing 1 year of topiramate treatment (N = 38). Physiological and metabolic measures were analyzed for correlation with weight loss during topiramate treatment. Results: In patients who completed 1 year of topiramate treatment, baseline weight was reduced in 82% at 3 months and in 86% at 1 year. Mean body weight was reduced 3.0 kg (3.9% of baseline) at 3 months and 5.9 kg (7.3%) at 1 year. In obese patients [body mass index (BMI) ≥ 30 kg/m²], mean weight loss was 4.2 kg (4.3%) at 3 months and 10.9 kg (11.0%) at 1 year. Weight loss was primarily caused by reduction in body fat mass. For all patients, weight loss at 3 months correlated most strongly with reduced caloric intake (p = 0.02). At 1 year, caloric intake had returned to baseline levels; weight loss correlated most strongly with higher baseline BMI (p = 0.0007). Discussion: Our results suggest that weight loss occurs in most adults treated with topiramate and is sustained for at least 1 year. Reduced caloric intake may account, in part, for weight loss during early treatment. The pattern of weight loss differs according to baseline BMI, with obese patients experiencing greater weight loss during continued therapy.     

QUERCETIN EFFECTS ON WEIGHT GAIN AND CALORIC INTAKE IN EXERCISED RATS

Quercetin is a flavonoid which activates oxidative metabolism. Quercetin may reduce weight gain by decreasing feed efficiency. The present study aims to evaluate weight gain, caloric intake and feed efficiency in exercised and sedentary rats supplemented with quercetin. Wistar rats were divided into four groups: quercetin-exercise training (QT), quercetin-sedentary (QS), placebo-exercise training (PT) and placebo-sedentary (PS). Rats were exercised and/or orally supplemented with quercetin (25 mg · kg⁻¹ on alternate days) during six weeks. Weight gain of the QT group decreased when compared with the PT and PS groups. Exercised groups increased cumulative caloric intake during the experimental period. The QT group rats also reduced their feed efficiency when compared with the QS and PS groups. These results suggest that quercetin is not able to decrease weight gain because no differences were found between placebo and quercetin condition either in the sedentary or in the training condition.     

Drinking water is associated with weight loss in overweight dieting women independent of diet and activity

Background: Data from short‐term experiments suggest that drinking water may promote weight loss by lowering total energy intake and/or altering metabolism. The long‐term effects of drinking water on change in body weight and composition are unknown, however. Objective: This study tested for associations between absolute and relative increases in drinking water and weight loss over 12 months. Methods and Procedures: Secondary analyses were conducted on data from the Stanford A TO Z weight loss intervention on 173 premenopausal overweight women (aged 25–50 years) who reported <1 l/day drinking water at baseline. Diet, physical activity, body weight, percent body fat (dual‐energy X‐ray absorptiometry), and waist circumference were assessed at baseline, 2, 6, and 12 months. At each time point, mean daily intakes of drinking water, noncaloric, unsweetened caloric (e.g., 100% fruit juice, milk) and sweetened caloric beverages, and food energy and nutrients were estimated using three unannounced 24‐h diet recalls. Beverage intake was expressed in absolute (g) and relative terms (% of beverages). Mixed models were used to test for effects of absolute and relative increases in drinking water on changes in weight and body composition, controlling for baseline status, diet group, and changes in other beverage intake, the amount and composition of foods consumed and physical activity. Results: Absolute and relative increases in drinking water were associated with significant loss of body weight and fat over time, independent of covariates. Discussion: The results suggest that drinking water may promote weight loss in overweight dieting women.     

Daily ration estimates for yellowfin sole, Limanda aspera (Pallas), based on laboratory consumption and growth

Several estimates of minimal energy requirements for yellowfin sole were made. Energy expenditures of 1.6, 4.1 and 8.3 cal g⁻¹ day⁻¹ were obtained from starvation weight loss, standard metabolism and maintenance ration procedures, respectively, at 6° C. The temperature effect on energy requirement was reflected in the Q ₁₀ values for starvation weight loss (2.0), standard metabolism (6.3) and maintenance ration (6.5).
Both energy intake and weight of food were linearly related to, and good predictors of, laboratory growth. These relationships were used to estimate the food and energy intake necessary for yellowfin sole to achieve a year's growth in the natural environment. Based on a caloric value of 2.0 kcal g⁻¹ of food (herring fillets), yellowfin would require 0.35 to 0.39% body weight day⁻¹ at 3° C to achieve the mean growth rate exhibited in the Bering Sea. To achieve Gulf of Alaska growth rates at 5 to 6° C, yellowfin would require 0.63% body weight day⁻¹. Based on a caloric value of 0.57 kcal g⁻¹ of food (chopped octopus), yellowfin would require 0.83% body weight per day to achieve the Gulf of Alaska growth rate (6° C). These requirements based on the calorific value of herring fillets, which are three to five times higher than previous estimates of daily ration in this species, are probably conservative estimates since many of their prey species have a lower energy content.     

Effect of weight loss on some serum cytokines in human obesity: increase in IL-10 after weight loss

Obesity is a major risk factor for hypertension, coronary artery disease and type 2 diabetes. Weight loss is associated with significant metabolic benefits. Our objective was to examine changes in adipocytokines and interleukin (IL) 10 in obese subjects before and after weight loss. We measured anthropometric parameters, adipocytokine and IL-10 in 78 obese people who had visited obesity clinics at five university hospitals (Ajou, Ulsan, Catholic, Hanyang and Yonsei) in Korea. They restricted their caloric intake to less than their usual intake (by 500 kcal), were administered sibutramine and were given a program of exercise for 12 weeks. After 12 weeks, weight, body mass index, waist circumference, hip circumference, waist-to-hip ratio, total body fat, total cholesterol, triglyceride, tumor necrosis factor alpha (TNF-alpha), IL-6, resistin and leptin had significantly decreased, while adiponectin and IL-10 had significantly increased. A bivariate correlation analysis found that increment in IL-10 and baseline IL-10 levels significantly correlated with decrement in TNF-alpha (P<.01) and baseline adiponectin (r=.52, P<.001), respectively. These results were confirmed in a multiple regression analysis. The results suggest that weight loss after caloric restriction and medical treatment in obesity can improve metabolic risk factors through changes in some cytokines.     

The effects of sympathectomy and dexamethasone in rats ingesting sucrose

Both high-sucrose diet and dexamethasone (D) treatment increase plasma insulin and glucose levels and induce insulin resistance. We showed in a previous work (Franco-Colin, et al. Metabolism 2000; 49:1289-1294) that combining both protocols for 7 weeks induced less body weight gain in treated rats without affecting mean daily food intake. Since such an effect may be explained by an increase in caloric expenditure, possibly due to activation of the sympathetic nervous system by sucrose ingestion, in this work, and using 10% sucrose in the drinking water, male Wistar rats were divided into 4 groups. Two groups were sympathectomized using guanethidine (Gu) treatment for 3 weeks. One of these groups of rats received D in the drinking water. Of the 2 groups not receiving Gu, one was the control (C) and the other received D. After 8 weeks a glucose tolerance test was done. The rats were sacrificed and liver triglyceride (TG), perifemoral muscle lipid, and norepinephrine (NE) levels in the liver spleen, pancreas, and heart were determined. Gu-treated rats (Gu and Gu+D groups) showed less than 10% NE concentration compared to C and D rats, less daily caloric intake and body-weight gain, more sucrose intake, and better glucose tolerance. The area under the curve after glucose administration correlated significantly with the mean body weight gain of the rats, except for D group. Groups D (D and Gu+D) also showed less caloric intake and body-weight gain but higher liver weight and TG concentration and lower peripheral muscle mass. The combination of Gu+D treatments showed some peculiar results: negative body weight gain, a fatty liver, and low muscle mass. Though the glucose tolerance test had the worst results for the D group, it showed the best results in the Gu+D group. There were significant interactions for Guan X Dex by two-way ANOVA test for the area under the curve in the glucose tolerance test, muscle mass, and muscle lipids. The results suggest that dexamethasone catabolic effect is not caused by sympathetic activation.     

Neuropeptide Y (NPY) Y2 receptor-selective agonist inhibits food intake and promotes fat metabolism in mice: combined anorectic effects of Y2 and Y4 receptor-selective agonists

Peripheral administration of the endogenous Y(2) and Y(4) receptor selective agonists, PYY(3-36) and PP, have been shown to inhibit food intake and body weight gain in rodents, and to reduce appetite and caloric intake in humans. We have previously developed a long-acting, potent and highly selective Y(2) receptor selective agonist, N-alpha-Ac-[Nle(24,28), Trp(30), Nva(31), Psi(35-36)]PYY(22-36)-NH(2) (BT-48). BT-48 (ip) dose-dependently inhibited ad lib food intake and also decreased the respiratory quotient in mice during both the light and dark periods. The latter observation is indicative of enhanced fat metabolism. Moreover, BT-48 also inhibited food intake in fasted mice. Combined ip administration of BT-48 (50nmol/mouse) with a highly potent and selective Y(4) anorectic peptide, BVD-74D (50nmol/mouse), resulted in a powerful and long lasting inhibitory effect on food intake. As expected, this inhibitory effect on food intake was nearly double that exhibited by either peptide (50nmol/mouse) alone. In summary, BT-48, unlike PYY(3-36), exhibits little or no affinity to other "Y" receptors, and may therefore have a better clinical potential than PYY(3-36) for control of food intake. Moreover, it appears that treatment with a combination of Y(2) and Y(4) receptor selective agonists may constitute a more powerful approach to control food intake than treatment with either of these agonists alone.     

Senescent terminal weight loss in the male F344 rat

Loss of weight, often of unknown cause and culminating in death, commonly occurs in humans at advanced ages. Rats that live to old ages, such as the Fischer 344 (F344) strain, also exhibit a terminal loss in body weight. A presently held hypothesis is that the terminal weight loss in the F344 rat model is due to reduced food intake because of an alteration in hypothalamic function resulting in early satiation. We report findings on terminal weight loss and food intake in male F344 rats fed ad libitum (AL group) or a life-prolonging dietary regimen in which caloric intake was restricted (DR group). Rats in both dietary groups that did not exhibit a terminal weight loss died at younger ages than those exhibiting the loss. Terminal weight loss in the AL group was not associated with decreased food intake; indeed, half of the rats in this group had an increased food intake during the period of terminal weight loss. This finding is not in accord with the presently held hypothesis. In the DR group, terminal weight loss was associated with reduced food intake. Pathology (renal disease and neoplasms) did not explain the presence or absence of the association between reduced food intake and weight loss in either dietary group. The duration of the period of terminal weight loss was similar for the AL and DR groups. Apparently, restricting calories delays the occurrence but does not affect the duration of senescent terminal weight loss.     

Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice

Obesity and cigarette smoking are both important risk factors for insulin resistance, cardiovascular disease, and cancer. Smoking reduces appetite, which makes many people reluctant to quit. Few studies have documented the metabolic impact of combined smoke exposure (se) and high-fat-diet (HFD). Neuropeptide Y (NPY) is a powerful hypothalamic feeding stimulator that promotes obesity. We investigated how chronic se affects caloric intake, adiposity, plasma hormones, inflammatory mediators, and hypothalamic NPY peptide in animals fed a palatable HFD. Balb/c mice (5 wk old, male) were exposed to smoke (2 cigarettes, twice/day, 6 days/wk, for 7 wk) with or without HFD. Sham-exposed mice were handled similarly without se. Plasma leptin, hypothalamic NPY, and adipose triglyceride lipase (ATGL) mRNA were measured. HFD induced a 2.3-fold increase in caloric intake, increased adiposity, and glucose in both sham and se cohorts. Smoke exposure decreased caloric intake by 23%, with reduced body weight in both dietary groups. Fat mass and glucose were reduced only by se in the chow-fed animals. ATGL mRNA was reduced by HFD in se animals. Total hypothalamic NPY was reduced by HFD, but only in sham-exposed animals; se increased arcuate NPY. We conclude that although se ameliorated hyperphagia and reversed the weight gain associated with HFD, it failed to reverse fat accumulation and hyperglycemia. The reduced ATGL mRNA expression induced by combined HFD and se may contribute to fat retention. Our data support a powerful health message that smoking in the presence of an unhealthy Western diet increases metabolic disorders and fat accumulation.     

Growth and feeding relationships of a hand-reared lowland gorilla infant (Gorilla g gorilla)

A captive-born female lowland gorilla that was being hand-reared by a group of surrogate mothers in a public zoo was observed for her first 6 mo. Caloric intake and weight gain, along with feeding bias of surrogate mothers, were examined. Caloric intake was highest during early morning and late at night. The weekly caloric intake and weight gain fluctuated with no established pattern. Although the gorilla's caloric intake did not increase with age, her total weight increased with a slower growth rate in the latter part of the study period, indicating a decreased caloric intake/weight ratio. It became evident that each surrogate exhibited an “overfeeding” and “underfeeding” tendency; calories given by the surrogates varied considerably, reflecting the interaction between the infant and the surrogates.     

Intermittent Moderate Energy Restriction Improves Weight Loss Efficiency in Diet-Induced Obese Mice

Background

Intermittent severe energy restriction is popular for weight management. To investigate whether intermittent moderate energy restriction may improve this approach by enhancing weight loss efficiency, we conducted a study in mice, where energy intake can be controlled.

Methods

Male C57/Bl6 mice that had been rendered obese by an ad libitum diet high in fat and sugar for 22 weeks were then fed one of two energy-restricted normal chow diets for a 12-week weight loss phase. The continuous diet (CD) provided 82% of the energy intake of age-matched ad libitum chow-fed controls. The intermittent diet (ID) provided cycles of 82% of control intake for 5–6 consecutive days, and ad libitum intake for 1–3 days. Weight loss efficiency during this phase was calculated as (total weight change) ÷ [(total energy intake of mice on CD or ID)–(total average energy intake of controls)]. Subsets of mice then underwent a 3-week weight regain phase involving ad libitum re-feeding.

Results

Mice on the ID showed transient hyperphagia relative to controls during each 1–3-day ad libitum feeding period, and overall ate significantly more than CD mice (91.1±1.0 versus 82.2±0.5% of control intake respectively, n = 10, P<0.05). There were no significant differences between CD and ID groups at the end of the weight loss or weight regain phases with respect to body weight, fat mass, circulating glucose or insulin concentrations, or the insulin resistance index. Weight loss efficiency was significantly greater with ID than with CD (0.042±0.007 versus 0.018±0.001 g/kJ, n = 10, P<0.01). Mice on the CD exhibited significantly greater hypothalamic mRNA expression of proopiomelanocortin (POMC) relative to ID and control mice, with no differences in neuropeptide Y or agouti-related peptide mRNA expression between energy-restricted groups.

Conclusion

Intermittent moderate energy restriction may offer an advantage over continuous moderate energy restriction, because it induces significantly greater weight loss relative to energy deficit in mice.     

Short‐Term Effects of Gastric Bypass Surgery on Circulating Ghrelin Levels

Objective: To prospectively evaluate the short‐term effects of Roux‐en‐Y gastric bypass (RYGBP) on ghrelin secretion and its relevance on food intake and body weight changes. Research Methods and Procedures: Ghrelin response to a standardized test meal was evaluated in eight obese patients (BMI, 43.5 to 59.1 kg/m²) before and 6 weeks after RYGBP. Ghrelin response was compared with that of an age‐matched group of six normal weight individuals (BMI, 19.6 to 24.9 kg/m²). Results: Fasting serum ghrelin levels were lower in obese subjects compared with controls (p < 0.05). Meal ingestion significantly suppressed ghrelin concentration in controls (p < 0.05) and obese subjects (p < 0.05), albeit to a lesser degree in the latter group (p < 0.05). Despite a 10.3 ± 1.5% weight loss, fasting serum ghrelin levels were paradoxically further decreased in obese subjects 6 weeks after RYGBP (p < 0.05). Moreover, at this time‐point, food intake did not elicit a significant ghrelin suppression. The changes in ghrelin secretion after RYGBP correlated with changes in insulin sensitivity (p < 0.05) and caloric intake (p < 0.05). Discussion: This study showed that the adaptive response of ghrelin to body weight loss was already impaired 6 weeks after RYGBP. Our study provides circumstantial evidence for the potential role of ghrelin in the negative energy balance in RYGBP‐operated patients.     

Influence of weekend lifestyle patterns on body weight

Objective: To determine whether alterations in diet and/or activity patterns during weekends contribute to weight gain or hinder weight loss. Methods and Procedures: Randomized, controlled trial comparing 1 year of caloric restriction (CR) with 1 year of daily exercise (EX). Subjects included 48 healthy adults (30F, 18M) aged 50–60 years with BMI 23.5–29.9 kg/m². Body weight was measured on 7 consecutive mornings for a total of 165 weeks at baseline and 437 weeks during the 1‐year interventions. Daily weight changes were calculated for weekends (Friday to Monday) and weekdays (Monday to Friday). Daily energy intake was estimated using food diaries; daily physical activity was measured using accelerometers. Both measures were validated against doubly labeled water (DLW). Results: At baseline, participants consistently gained weight on weekend days (+0.06 ± 0.03 kg/day, (mean ± s.e.), P = 0.02), but not on weekdays (?0.02 ± 0.02 kg/day, P = 0.18). This was attributable to higher dietary intake on Saturdays and lower physical activity on Sundays relative to weekdays (both P < 0.05). During the interventions, both CR and EX participants were in negative energy balance on weekdays (P < 0.005). On weekends, however, CR participants stopped losing weight, and EX participants gained weight (+0.08 ± 0.03 kg/day, P < 0.0001) due to higher dietary intakes on weekends. This helps to explain the slower‐than‐expected rate of weight loss during the interventions. Discussion: Alterations in lifestyle behaviors on weekends contribute to weight gain or cessation of weight loss on weekends. These results provide one explanation for the relatively slow rates of weight loss observed in many studies, and the difficulty with maintaining significant weight loss.     

A combined healthy strategy for successful weight loss,weight maintenance and improvement of hepatic lipid metabolism

Obesity is critically related with the development of metabolic and pathophysiological alterations among which non-alcoholic fatty liver disease (NAFLD) is of especial relevance. Although there are numerous strategies to successfully treat obesity, the prevention of weight regain still remains challenging for individuals who have undergone weight loss programs. In such context, diet and physical activity are considered essential for the regulation of body weight and lipid metabolism. In this study, rats were fed a high-fat diet (HFD) to induce obesity and alterations in hepatic lipid metabolism. Obese rats were then treated with single or combined strategies of caloric restriction, physical exercise, and/or pharmacological treatment with an appetite suppressant, to lose weight, reverse the obesity-related alterations in hepatic morphology and lipid metabolism and maintain the beneficial effects of the interventions used. HFD induced excess body weight, hepatic steatosis, altered fatty acid profile, dysregulated gene expression of lipogenic and lipolytic enzymes, as well as plasma markers of liver damage, and modifications in liver antioxidant enzyme activity. Such alterations were ameliorated by caloric restriction in combination with a mixed training protocol and/or food-intake inhibitor administration during a weight loss intervention period of 3 weeks, and the beneficial effects remained after 6 weeks of weight maintenance, with some interesting interactions observed. In conclusion, weight loss strategies assayed were efficient at correcting the obesogenic action of a HFD and related alterations in hepatic functionality through different molecular mechanisms. The beneficial effects were also evident along the post-intervention maintenance period to avoid body weight regain.     

The parental origin of the single X chromosome in Turner syndrome: lack of correlation with parental age or clinical phenotype.

We have used X- and Y-linked RFLPs to determine the origin of the single X chromosome in 25 live-born individuals with Turner syndrome. We determined that 18 individuals retained a maternal X (Xm) and that seven retained the paternal X (Xp). No occult mosaicism was detected. We found no differences in either maternal or paternal ages for the two groups. The ratio of maternal X to paternal X is just over 2:1, which is consistent with the expected proportion of meiotic or mitotic products, with equal loss at each step, given the nonviability of 45,Y. Six phenotypic or physiologic characteristics were assessed: (1) birth weight, (2) height percentile at time of testing, (3) presence of a webbed neck, (4) cardiovascular abnormalities, (5) renal abnormalities, and (6) thyroid autoimmunity. There were no significant differences in birth weights or heights between the girls who retained the maternal X or the paternal X. In addition, no differences between the groups could be appreciated in the incidence of the physical, anatomic, or physiologic parameters assessed.     

Regulation of hypothalamic NPY by diet and smoking

Appetite is regulated by a number of hypothalamic neuropeptides including neuropeptide Y (NPY), a powerful feeding stimulator that responds to feeding status, and drugs such as nicotine and cannabis. There is debate regarding the extent of the influence of obesity on hypothalamic NPY. We measured hypothalamic NPY in male Sprague-Dawley rats after short or long term exposure to cafeteria-style high fat diet (32% energy as fat) or laboratory chow (12% fat). Caloric intake and body weight were increased in the high fat diet group, and brown fat and white fat masses were significantly increased after 2 weeks. Hypothalamic NPY concentration was only significantly decreased after long term consumption of the high fat diet. Nicotine decreases food intake and body weight, with conflicting effects on hypothalamic NPY reported. Body weight, plasma hormones and brain NPY were investigated in male Balb/c mice exposed to cigarette smoke for 4 days, 4 and 12 weeks. Food intake was significantly decreased by smoke exposure (2.32+/-0.03g/24h versus 2.71+/-0.04g/24h in control mice (non-smoke exposed) at 12 weeks). Relative to control mice, smoke exposure led to greater weight loss, while pair-feeding the equivalent amount of chow caused an intermediate weight loss. Chronic smoke exposure, but not pair-feeding, was associated with decreased hypothalamic NPY concentration, suggesting an inhibitory effect of cigarette smoking on brain NPY levels. Thus, consumption of a high fat diet and smoke exposure reprogram hypothalamic NPY. Reduced NPY may contribute to the anorexic effect of smoke exposure.     

Effects of a chronic wasting infection on skeletal muscle size and contractile properties

To evaluate the effects of chronic infection on skeletal muscle dimensions and contractile properties, we used a hamster model of visceral leishmaniasis, a parasitic infection of the reticuloendothelial system produced by Leishmania donovani (LD). To distinguish between effects of reduced caloric intake and infection per se, we also studied healthy control animals and noninfected animals subjected to caloric restriction. Three muscles were tested in vitro: plantaris, soleus, and diaphragm. Both caloric restriction and LD infection caused loss of body weight and reduced muscle cross-sectional areas and wet weights. The interventions had variable effects on in vitro contractile properties, the most pronounced being reduction in peak tension in response to tetanic stimulation. Tension loss was 35-45%, except for a loss of 65% in plantaris of LD-infected animals. We conclude that chronic LD infection affects skeletal muscles in both indirect and direct ways. 1) Reduced caloric intake due to anorexia decreases muscle size and active tension. Disuse probably enhances this effect in limb muscles. 2) Infection produces profound weakness of inactive fast-twitch muscle by unknown mechanisms.