scholarly journals Rimonabant prevents additional accumulation of visceral and subcutaneous fat during high-fat feeding in dogs

2009 ◽  
Vol 296 (6) ◽  
pp. E1311-E1318 ◽  
Author(s):  
Joyce M. Richey ◽  
Orison O. Woolcott ◽  
Darko Stefanovski ◽  
L. Nicole Harrison ◽  
Dan Zheng ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Metabolic Rate ◽  
Resting Metabolic Rate ◽  
Subcutaneous Fat ◽  
Body Weight Loss ◽  
Weight Changes ◽  
High Fat ◽  
Body Weight Changes

We investigated whether rimonabant, a type 1 cannabinoid receptor antagonist, reduces visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) in dogs maintained on a hypercaloric high-fat diet (HHFD). To determine whether energy expenditure contributed to body weight changes, we also calculated resting metabolic rate. Twenty male dogs received either rimonabant (1.25 mg·kg−1·day−1, orally; n = 11) or placebo ( n = 9) for 16 wk, concomitant with a HHFD. VAT, SAT, and nonfat tissue were measured by magnetic resonance imaging. Resting metabolic rate was assessed by indirect calorimetry. By week 16 of treatment, rimonabant dogs lost 2.5% of their body weight ( P = 0.029), whereas in placebo dogs body weight increased by 6.2% ( P < 0.001). Rimonabant reduced food intake ( P = 0.027), concomitant with a reduction of SAT by 19.5% ( P < 0.001). In contrast with the VAT increase with placebo ( P < 0.01), VAT did not change with rimonabant. Nonfat tissue remained unchanged in both groups. Body weight loss was not associated with either resting metabolic rate ( r2 = 0.24; P = 0.154) or food intake ( r2 = 0.24; P = 0.166). In conclusion, rimonabant reduced body weight together with a reduction in abdominal fat, mainly because of SAT loss. Body weight changes were not associated with either resting metabolic rate or food intake. The findings provide evidence of a peripheral effect of rimonabant to reduce adiposity and body weight, possibly through a direct effect on adipose tissue.

scholarly journals The effects of enterostatin intake on food intake and energy expenditure

2003 ◽  
Vol 90 (1) ◽  
pp. 207-214 ◽  
Author(s):  
Eva M. R. Kovacs ◽  
Manuela P. G. M. Lejeune ◽  
Margriet S. Westerterp-Plantenga
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Resting Metabolic Rate ◽  
Body Weight Loss ◽  
Negative Energy ◽  
High Fat ◽  
Double Blind ◽  
Diet Induced Thermogenesis

Enterostatin (ENT) has been found to inhibit food intake and selectively inhibit fat intake in rats. Both peripheral and central mechanisms have been proposed. It also has been suggested that ENT may increase thermogenesis. The present study investigated the effects of oral ENT administration on food intake, energy expenditure and body weight in subjects with a preference for a high-fat diet. In a double-blind, placebo-controlled, randomized and crossover design, nine female and three male healthy subjects (age 34 (sd 11) years, BMI 24·5 (sd 2·5) kg/m2) with a preference for a high-fat diet ingested ENT (3 × 15 mg/d) or placebo (PLA) while consuming a high-fat diet ad libitum for 4d. Eight subjects ended each intervention with a 36h stay in the respiration chamber, continuing the diet and treatment. Body-weight loss was significant (ENT 0·8 (se 0·3) kg, P<0·05; PLA 1·3 (se 0·3) kg, P<0·001), but not different between treatments. There was no difference between treatments in total energy intake (ENT 37·1 (se 2·6), PLA 35·9 (se 3·2) MJ), macronutrient composition, hunger, satiety and hedonic scores during the 4d high-fat diet. Energy expenditure (24h) (ENT 9·6 (se 0·4), PLA 9·5 (se 0·4) MJ), sleeping and resting metabolic rate, diet-induced thermogenesis, activity-induced energy expenditure and 24h RQ (ENT 0·77 (se 0·01), PLA 0·77 (se 0·01)) were similar for both treatments. We conclude that oral ENT administration did not affect food intake, energy expenditure or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance.

Adiponectin is required to mediate rimonabant-induced improvement of insulin sensitivity but not body weight loss in diet-induced obese mice

2009 ◽  
Vol 296 (4) ◽  
pp. R929-R935 ◽  
Author(s):  
Stéphanie Migrenne ◽  
Amélie Lacombe ◽  
Anne-Laure Lefèvre ◽  
Marie-Pierre Pruniaux ◽  
Etienne Guillot ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Energy Homeostasis ◽  
Hepatic Glucose Production ◽  
Body Weight Loss ◽  
Metabolic Effects ◽  
Wild Type ◽  
High Fat ◽  
Wild Type Littermate

The increase in adiponectin levels in obese patients with untreated dyslipidemia and its mRNA expression in adipose tissue of obese animals are one of the most interesting consequences of rimonabant treatment. Thus, part of rimonabant's metabolic effects could be related to an enhancement of adiponectin secretion and its consequence on the modulation of insulin action, as well as energy homeostasis. The present study investigated the effects of rimonabant in adiponectin knockout mice (Ad−/−) exposed to diet-induced obesity conditions. Six-week-old Ad−/− male mice and their wild-type littermate controls (Ad+/+) were fed a high-fat diet for 7 mo. During the last month, animals were administered daily either with vehicle or rimonabant by mouth (10 mg/kg). High-fat feeding induced weight gain by about 130% in both wild-type and Ad−/− mice. Obesity was associated with hyperinsulinemia and insulin resistance. Treatment with rimonabant led to a significant and similar decrease in body weight in both Ad+/+ and Ad−/− mice compared with vehicle-treated animals. In addition, rimonabant significantly improved insulin sensitivity in Ad+/+ mice compared with Ad+/+ vehicle-treated mice by decreasing hepatic glucose production and increasing glucose utilization index in both visceral and subcutaneous adipose tissue. In contrast, rimonabant failed to improve insulin sensitivity in Ad−/− mice, despite the loss in body weight. Rimonabant's effect on body weight appeared independent of the adiponectin pathway, whereas adiponectin seems required to mediate rimonabant-induced improvement of insulin sensitivity in rodents.

Sex Differences in Severity of Inflammation-Induced Anorexia and Weight Loss

2004 ◽  
Vol 5 (4) ◽  
pp. 255-264 ◽  
Author(s):  
Terry A. Lennie
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Sex Differences ◽  
Food Intake ◽  
Acute Inflammation ◽  
Sesame Oil ◽  
Female Rats ◽  
Male Rats ◽  
Weight Changes ◽  
Body Weight Changes

Food intake and body weight changes in response to induction of acute inflammation were examined in intact cycling females, ovariectomized females, and sham-operated male rats. In intact females, body weight and feeding responses were compared between rats in which inflammation was induced on day of estrus with rats in which inflammation was induced on day of diestrus. Anorexia and weight loss were more severe in the female rats with inflammation induced on estrus day, which coincides with peak serum estrogen levels. In ovariectomized females, inflammation was induced the day after rats received injections of estrogen, progesterone, or sesame oil (vehicle). Males received vehicle injections. Among female rats, the group that received estradiol injections the previous day displayed the most severe anorexia. The least severe anorexia was observed in female rats that received progesterone the previous day. Food intake of female rats that received vehicle injections prior to induction of inflammation was greater than the rats receiving estrogen but less than the rats receiving progesterone. Male rats displayed the most severe anorexia and greatest weight loss. These data suggest that, although females exposed to estradiol prior to induction of acute inflammation display more severe anorexia than those exposed to progesterone, it may be that progesterone attenuates severity of anorexia rather than estrogen solely potentiating severity. Male rats, however, appear to experience the most severe anorexia in response to this form of inflammation.

Ventromedial hypothalamic knife-cut lesions in rats resistant to dietary obesity

1984 ◽  
Vol 246 (6) ◽  
pp. R943-R948 ◽  
Author(s):  
J. Oku ◽  
G. A. Bray ◽  
J. S. Fisler ◽  
R. Schemmel
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
High Fat Diet ◽  
Corn Oil ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Dietary Obesity

The effects of ventromedial hypothalamic (VMH) knife-cut lesions on food intake and body weight of S 5B/Pl rats, which are normally resistant to obesity when eating a high-fat diet, were examined in two experiments. In the first experiment body weight increased only slightly after VMH knife-cut lesions when animals were fed pelleted laboratory chow or a 10% corn oil diet. When eating the 30% corn oil diet, however, body weight increased in the VMH knife-cut rats. In the second experiment VMH knife-cut lesions produced a small weight gain in rats fed the 10% fat diet; this manipulation also increased food intake and disrupted the normal diurnal feeding pattern. Changes in the weight of the liver, interscapular brown adipose tissue, and white adipose tissue paralleled the changes in body weight. Plasma insulin increased in the rats eating the 30% corn oil diet ad libitum but not in the VMH-lesioned animals pair fed to the sham-operated rats. Incorporation of 3H from 3H2O into lipid was significantly increased in white fat of animals with VMH knife cuts. Similar results were obtained from incubation of adipose tissue in vitro with insulin and radioactively labeled glucose. These studies show that hypothalamic knife-cut lesions can remove the resistance of the S 5B/Pl rats to obesity when they are fed a high-fat diet.

High-fat diet induces site-specific unresponsiveness to LPS-stimulated STAT3 activation in the hypothalamus

2014 ◽  
Vol 306 (1) ◽  
pp. R34-R44 ◽  
Author(s):  
Beatriz de Carvalho Borges ◽  
Rodrigo Rorato ◽  
Ernane Torres Uchoa ◽  
Paula Marangon ◽  
Glauber S. F. da Silva ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Brain Stem ◽  
High Fat Diet ◽  
Control Diet ◽  
Body Weight Loss ◽  
Hypothalamic Nucleus ◽  
High Fat

Hypophagia induced by inflammation is associated with Janus kinase (JAK)-2/signal transducer and activator of transcription (STAT) 3 signaling pathway, and leptin-mediated hypophagia is also mediated by JAK2-STAT3 pathway. We have previously reported that lipopolysaccharide (LPS) did not reduce food intake in leptin-resistant high-fat diet (HFD) rats but maintained body weight loss. We investigated whether changes in p-STAT3 expression in the hypothalamus and brain stem could account for the desensitization of hypophagia in HFD animals after a low LPS dose (100 μg/kg). Wistar rats fed standard diet (3.95 kcal/g) or HFD (6.3 kcal/g) for 8 wk were assigned into control diet-saline, control diet-LPS, HFD-saline, and HFD-LPS groups. LPS reduced feeding in the control diet but not HFD. This group showed no p-STAT3 expression in the paraventricular nucleus (PVN) and ventromedial hypothalamic nucleus (VMH), but sustained, though lower than control, p-STAT3 in the nucleus of the solitary tract (NTS) and raphe pallidus (RPa). LPS decreased body weight in HFD rats and increased Fos expression in the NTS. LPS increased body temperature, oxygen consumption, and energy expenditure in both control diet and HFD rats, and this response was more pronounced in HFD-LPS group. Brown adipose tissue (BAT) thermogenesis and increased energy expenditure seem to contribute to body weight loss in HFD-LPS. This response might be related with increased brain stem activation. In conclusion, LPS activates STAT3-mediated pathway in the hypothalamus and brain stem, leading to hypophagia, however, LPS effects on food intake, but not body weight loss, are abolished by leptin resistance induced by HFD. The preserved STAT3 phosphorylation in the brain stem suggests that unresponsiveness to LPS on STAT3 activation under HFD might be selective to the hypothalamus.

scholarly journals Two-year follow-up cohort study focused on gender-specific associations between socioeconomic status and body weight changes in overweight and obese middle-aged and older adults

BMJ Open ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. e050127
Author(s):  
Malgorzata Biskup ◽  
Pawel Macek ◽  
Stanislaw Gozdz ◽  
Malgorzata Terek-Derszniak ◽  
Halina Krol ◽  
...  
Keyword(s):  
Socioeconomic Status ◽  
Weight Loss ◽  
Body Weight ◽  
Low Income ◽  
Body Weight Loss ◽  
Occupational Activity ◽  
Weight Changes ◽  
Body Weight Changes ◽  
Gender Specific

ObjectiveAs overall spread of obesity in populations is generally acknowledged to result from unhealthy lifestyles rather than individual genetic makeup, this study aimed to gain specific insights into its determinants through assessing the prevalent associations between individual socioeconomic status (SES) and weight loss in overweight and obese men and women.MethodsA prospective, 2-year follow-up study covered 3362 (38.0% men) respondents, aged 43–64 years, body mass index ≥25 kg/m2. Changes in body weight were estimated as a percentage of initial weight. Three categories of changes were defined: gained ≥3%, stable (gained <3% or lost <3%), lost ≥3%. Body weight loss was determined against three categories: lost ≥3 to <5%, lost ≥5 to <10%, lost ≥10%. Select SES variables (ie, gender, age, education, marital status, occupational activity and income) were determined in line with the Health Status Questionnaire. The associations between SES and body weight changes were analysed with the aid of logistic regression models. The results were presented as ORs with 95% CIs.ResultsOnly 18% of the respondents had complied with the medical recommendations on weight loss. Significant differences were encountered between the gender, age and occupational activity variables and the weight loss one. Multifactorial models were used to determine the following gender-specific associations between SES and weight loss. Men with moderate income had significantly higher odds for weight loss (≈75%), as compared with the higher earners, whereas women with low income, occupationally inactive, had significantly higher odds (≈30% and ≈50%, respectively), as compared with the high earners and occupationally active ones.ConclusionsLower education, male gender, lower income per household, older age and unemployment status were the established factors predisposing to obesity. While aiming to ensure effectiveness of the measures specifically aimed at preventing obesity, population groups deemed most at risk of potential weight gain must prior be identified.

scholarly journals Coix seed oil ameliorates cancer cachexia by counteracting muscle loss and fat lipolysis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Huiquan Liu ◽  
Lu Li ◽  
Jun Zou ◽  
Ting Zhou ◽  
Bangyan Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Cancer Cachexia ◽  
Seed Oil ◽  
Body Weight Loss ◽  
Tissue Loss ◽  
Epididymal Adipose Tissue ◽  
Tnf Α ◽  
Coix Seed

Abstract Background Cancer cachexia is a cancer-induced multifactorial debilitating syndrome directly accounting for 20% of cancer deaths without effective therapeutic approaches. It is extremely urgent to explore effective anti-cachexia drugs to ameliorate muscle and fat loss in cachexia patients. Methods Lewis lung carcinoma bearing C57BL/6 mice were applied as the animal model to examine the therapeutic effect of Coix seed oil (CSO) on cancer cachexia. The food intake and body weight change were monitored every 3 days throughout the experiment. The IL-6 and TNF-α levels in serum were detected by ELISA assay. Several key proteins involved in muscle wasting and fat lipolysis were tested by Western blot to identify the potential mechanism of CSO. Results Administration of CSO through gavage significantly prevented body weight loss and ameliorated systemic inflammation without affecting food intake and tumor size. The weight and histological morphology of gastrocnemius muscle and epididymal adipose tissue in CSO-treated mice were also improved. In mechanism, we found that CSO decreased the expression of MuRF1 and the ratio of phospho-p65 (Ser536) to p65 in muscle tissue. Meanwhile, cancer-induced activation of HSL and AMPK was also inhibited by CSO administration. Conclusion Coix seed oil exerts an anti-cachexia pharmaceutical effect by counteracting muscle and adipose tissue loss most likely through regulating NF-κB-MuRF1 and AMPK-HSL pathway.

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