scholarly journals Sex and Genotype Dependent Effects of a Restricted Access Diet in Ghrelin-Deficient Mice

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A56-A56
Author(s):  
Karina Prins ◽  
Patric J Delhanty ◽  
Martin Huisman ◽  
Rosinda Mies ◽  
Anke McLuskey ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Locomotor Activity ◽  
Food Intake ◽  
Energy Expenditure ◽  
Glucose Tolerance ◽  
Body Weight Gain ◽  
Light Phase ◽  
Male And Female ◽  
Restricted Access

Abstract Ghrelin, a peptide hormone secreted by the stomach, stimulates both appetite and reward signalling. Its deletion in mice results in poor recovery from metabolic challenges, like starvation, but does not affect food intake or body weight. While sex differences in appetite and feeding behavior have been reported, little is known about the role of ghrelin herein. To investigate this, we used a metabolic cage system to continuously monitor responses of ghrelin-deficient (GKO) and wildtype (WT) mice to three different diets. Male and female mice (5 weeks old) were housed individually in a Promethion system (Sable Systems, USA) and provided one of three diets for 9 weeks: RA, continuous chow with restricted access to a Western-style diet (WD; 2h access, 3d/week) in the light phase; CA, continuous access to both diets; CC, continuous chow. Glucose tolerance was assessed at week 7 by IPGTT; food intake (kcal/g bodyweight), energy expenditure and locomotor activity at week 8; body weight and body composition (EchoMRI, USA) at week 9. On access days, RA mice ate up to 60% of their 24h intake during the WD access period. Following WD access GKO RA mice ate less chow than WT RA mice. Intriguingly, this compensatory reduction in food intake by GKO mice occurred at different times for males and females. GKO RA males ate 45% less chow in the dark phase immediately after WD access (p < 0.001). In contrast, this reduction in food intake (30% less) did not occur until the following, non-access, day in GKO RA females (genotype-sex: p < 0.05). Depending on diet, GKO mice showed differential regulation of energy expenditure in the light phase. Energy expenditure was 6–17% higher in GKO than WT mice in the RA group on access days and in the CA group. On non-access days, however, GKO mice in the RA group expended 13% less energy than WT RA mice (p < 0.005). Regardless of diet, locomotor activity in females was greater than in males (p < 0.001). However, GKO females in the RA and CC groups showed a marked 30% reduction in locomotor activity compared to WTs (genotype-sex: p < 0.05). After nine weeks, neither sex nor genotype effects were seen in body weight gain and composition of RA animals. CA females gained 17% more body weight and had a 6.1% higher fat percentage than CA males (both p < 0.001). In the CC group body weight gain did not differ, but GKO females had 3.1% more fat than WT females (genotype-sex: p < 0.01). Glucose tolerance (AUC) was similar in all groups. In conclusion, we demonstrated that ghrelin deficiency changes the response to the three diets in a sex-dependent manner. Especially, restricted access to WD differentially affected food intake timing and locomotor activity of male and female GKO mice. These results add to the growing body of evidence that ghrelin signalling is sexually dimorphic.

Pharmacological actions of the peptide hormone amylin in the long-term regulation of food intake, food preference, and body weight

2007 ◽  
Vol 293 (5) ◽  
pp. R1855-R1863 ◽  
Author(s):  
Christine Mack ◽  
Julie Wilson ◽  
Jennifer Athanacio ◽  
James Reynolds ◽  
Kevin Laugero ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Locomotor Activity ◽  
Food Intake ◽  
Energy Expenditure ◽  
Food Preference ◽  
Body Weight Gain ◽  
The Body ◽  
High Fat

The ability of amylin to reduce acute food intake in rodents is well established. Longer-term administration in rats (up to 24 days) shows a concomitant reduction in body weight, suggesting energy intake plays a significant role in mediating amylin-induced weight loss. The current set of experiments further explores the long-term effects of amylin (4–11 wk) on food preference, energy expenditure, and body weight and composition. Furthermore, we describe the acute effect of amylin on locomotor activity and kaolin consumption to test for possible nonhomeostatic mechanisms that could affect food intake. Four-week subcutaneous amylin infusion of high-fat fed rats (3–300 μg·kg−1·day−1) dose dependently reduced food intake and body weight gain (ED50for body weight gain = 16.5 μg·kg−1·day−1). The effect of amylin on body weight gain was durable for up to 11 wks and was associated with a specific loss of fat mass and increased metabolic rate. The body weight of rats withdrawn from amylin (100 μg·kg−1·day−1) after 4 wks of infusion returned to control levels 2 wks after treatment cessation, but did not rebound above control levels. When self-selecting calories from a low- or high-fat diet during 11 wks of infusion, amylin-treated rats (300 μg·kg−1·day−1) consistently chose a larger percentage of calories from the low-fat diet vs. controls. Amylin acutely had no effect on locomotor activity or kaolin consumption at doses that decreased food intake. These results demonstrate pharmacological actions of amylin in long-term body weight regulation in part through appetitive-related mechanisms and possibly via changes in food preference and energy expenditure.

scholarly journals Effect of chronic infusion of olanzapine and clozapine on food intake and body weight gain in male and female rats

Life Sciences ◽  
2007 ◽  
Vol 81 (12) ◽  
pp. 1024-1030 ◽  
Author(s):  
SuJean Choi ◽  
Briana DiSilvio ◽  
JayLynn Unangst ◽  
John D. Fernstrom
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Chronic Infusion

scholarly journals Development of obesity in transgenic rats with low circulating growth hormone levels: involvement of leptin resistance

2000 ◽  
pp. 535-541 ◽  
Author(s):  
Y Furuhata ◽  
R Kagaya ◽  
K Hirabayashi ◽  
A Ikeda ◽  
KT Chang ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cerebrospinal Fluid ◽  
Body Weight ◽  
Weight Gain ◽  
Locomotor Activity ◽  
Food Intake ◽  
Body Weight Gain ◽  
Leptin Resistance ◽  
Intracerebroventricular Injection ◽  
Transgenic Rats

BACKGROUND: Human growth hormone (hGH) transgenic (TG) rats have been produced in our laboratory. These TG rats are characterized by low circulating hGH levels, virtually no endogenous rGH secretion, and massive obesity. OBJECTIVE: To elucidate how energy balance and leptin sensitivity contributed to the establishment of this obesity. DESIGN AND METHODS: Food intake, locomotor activity and leptin concentrations in serum and cerebrospinal fluid were measured in TG rats and their non-transgenic littermates (control). The effect of intraperitoneal and intracerebroventricular injection of leptin on food intake and body weight gain was also examined. RESULTS: An increase in food intake and a decrease in locomotor activity were observed from 4 and 7 weeks of age, respectively, in the transgenic rats compared with control. Serum leptin concentrations of the transgenic rats were more than twice as high as those of control rats and were associated with an increased white adipose tissue mass and ob gene expression. Intraperitoneal injection of leptin significantly decreased food intake and body weight gain in control rats, but not in transgenic rats. Leptin concentration in the cerebrospinal fluid of transgenic rats was not different from that of control rats, and intracerebroventricular injection of leptin was similarly effective in reducing food intake and body weight gain as it was in control rats. CONCLUSIONS: These results suggest that the transgenic rats, whose GH secretion is suppressed, develop obesity due to early onset of an increase in food intake and a decrease in locomotor activity with leptin resistance resulting from deteriorating leptin transport from peripheral blood to cerebrospinal fluid.

A specific dose of grape seed-derived proanthocyanidins to inhibit body weight gain limits food intake and increases energy expenditure in rats

2016 ◽  
Vol 56 (4) ◽  
pp. 1629-1636 ◽  
Author(s):  
Joan Serrano ◽  
Àngela Casanova-Martí ◽  
Andreu Gual ◽  
Anna Maria Pérez-Vendrell ◽  
M. Teresa Blay ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Energy Expenditure ◽  
Body Weight Gain ◽  
Grape Seed

Effects of not predictable alternative overcrowding and isolation on food intake and body weight gain in male and female rats at weaning or adulthood

Appetite ◽  
2010 ◽  
Vol 54 (3) ◽  
pp. 638
Author(s):  
A. Cárdenas ◽  
V.A. López-Espinoza ◽  
F. Díaz ◽  
A.G. Martínez ◽  
K. Franco-Paredes ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats

scholarly journals Pathophysiology of drug induced weight and metabolic effects: findings from an RCT in healthy volunteers treated with olanzapine, iloperidone, or placebo

2018 ◽  
Vol 32 (5) ◽  
pp. 533-540 ◽  
Author(s):  
Jacob S Ballon ◽  
Utpal B Pajvani ◽  
Laurel ES Mayer ◽  
Zachary Freyberg ◽  
Robin Freyberg ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Energy Expenditure ◽  
Glucose Tolerance ◽  
Healthy Volunteers ◽  
Second Generation ◽  
Metabolic Effects ◽  
Insulin Metabolism

Second generation antipsychotics are prescribed for an increasing number of psychiatric conditions, despite variable associations with weight gain, dyslipidemia, and impaired glucose tolerance. The mechanism(s) of the apparent causal relationships between these medications and metabolic effects have been inadequately defined and are potentially confounded by genetic risk of mental illness, attendant lifestyle, and concomitant medications. Therefore, we conducted a study in which 24 healthy volunteers were randomized to olanzapine (highly weight-gain liability), iloperidone (less weight-gain liability), or placebo treatment for 28 days under double-blind conditions. We hypothesized that antipsychotics induce weight gain primarily through increased caloric intake, which causes secondary dyslipidemia and insulin resistance. Subjects were phenotyped pre- and post-treatment for body weight, adiposity by dual energy X-ray absorptiometry, energy expenditure by indirect calorimetry, food intake, oral glucose tolerance, plasma lipids, glucose, insulin, and other hormones. We found significantly increased food intake and body weight but no change in energy expenditure in olanzapine-treated subjects, with associated trends towards lipid abnormalities and insulin resistance the extent of which were presumably limited by the duration of treatment. Iloperidone treatment led to modest non-significant and placebo no weightgain, lipid increases and alterations in insulin metabolism. We conclude that second generation antipsychotic drugs, as represented by olanzapine, produce their weight and metabolic effects, predominantly, by increasing food intake which leads to weight gain that in turn induces metabolic consequences, but also through other direct effects on lipid and glucose metabolism independant of food intake and weight gain.

scholarly journals A Functional Leptin System Is Essential for Sodium Tungstate Antiobesity Action

Endocrinology ◽  
2009 ◽  
Vol 150 (2) ◽  
pp. 642-650 ◽  
Author(s):  
Ignasi Canals ◽  
María C. Carmona ◽  
Marta Amigó ◽  
Albert Barbera ◽  
Analía Bortolozzi ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Energy Expenditure ◽  
Energy Homeostasis ◽  
Sodium Tungstate ◽  
Body Weight Gain ◽  
Dependent Manner ◽  
Leptin System

Sodium tungstate is a novel agent in the treatment of obesity. In diet-induced obese rats, it is able to reduce body weight gain by increasing energy expenditure. This study evaluated the role of leptin, a key regulator of energy homeostasis, in the tungstate antiobesity effect. Leptin receptor-deficient Zucker fa/fa rats and leptin-deficient ob/ob mice were treated with tungstate. In lean animals, tungstate administration reduced body weight gain and food intake and increased energy expenditure. However, in animals with deficiencies in the leptin system, treatment did not modify these parameters. In ob/ob mice in which leptin deficiency was restored through adipose tissue transplantation, treatment restored the tungstate-induced body weight gain and food intake reduction as well as energy expenditure increase. Furthermore, in animals in which tungstate administration increased energy expenditure, changes in the expression of key genes involved in brown adipose tissue thermogenesis were detected. Finally, the gene expression of the hypothalamic neuropeptides, Npy, Agrp, and Cart, involved in the leptin regulation of energy homeostasis, was also modified by tungstate in a leptin-dependent manner. In summary, the results indicate that the effectiveness of tungstate in reducing body weight gain is completely dependent on a functional leptin system. Anti-obesity activity of tungstate is due to an increase in thermogenesis and a reduction in food intake and depends entirely on a functional leptin system.

Deletion of PTP 1B from Brain Neurons Partly Protects Mice from Diet-Induced Obesity and Minimally Improves Fertility

Endocrinology ◽  
2021 ◽  
Author(s):  
Caroline M Ancel ◽  
Maggie C Evans ◽  
Romy I Kerbus ◽  
Elliot G Wallace ◽  
Greg M Anderson
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Glucose Tolerance ◽  
Knockout Mice ◽  
Body Weight Gain ◽  
Negative Regulator ◽  
Cytokine Signaling ◽  
Male And Female ◽  
Female Mice ◽  
Calorie Diet

Abstract Reproductive dysfunction in women has been linked to high calorie diet (HCD)-feeding and obesity. Central resistance to leptin and insulin have been shown to accompany diet-induced infertility in rodent studies, and we have previously shown that deleting suppressor of cytokine signaling 3, which is a negative regulator of leptin signaling, from all forebrain neurons partially protects mice from HCD-induced infertility. In this study, we were interested in exploring the role of protein tyrosine phosphatase 1B (PTP1B), which is a negative regulator of both leptin and insulin signaling, in the pathophysiology of HCD-induced obesity and infertility. To this end, we generated male and female neuron-specific PTP1B knockout mice and compared their body weight gain, food intake, glucose tolerance and fertility to control littermates under both normal calorie diet-feeding and HCD-feeding conditions. Both male and female mice with neuronal PTP1B deletion exhibited slower body weight gain in response to HCD-feeding, yet only male knockout mice exhibited improved glucose tolerance compared with controls. Neuronal PTP1B deletion improved the time to first litter in HCD-fed mice, but did not protect female mice from eventual HCD-induced infertility. While the mice fed a normal caloric diet remained fertile throughout the 150 day period of assessment, HCD-fed females became infertile after producing only a single litter, regardless of their genotype. These data show that neuronal PTP1B deletion is able to partially protect mice from HCD-induced obesity, but is not a critical mediator of HCD-induced infertility.

scholarly journals Soy Protein Health Benefits Are in Part Dependent of the Gut Microbiota

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 669-669
Author(s):  
Armando Tovar ◽  
Monica Sanchez-Tapia ◽  
Daniela Moreno ◽  
Guillermo Ordaz ◽  
Martha Guevara ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Expenditure ◽  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Antibiotic Treatment ◽  
Soy Protein ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
High Fat

Abstract Objectives Several studies have demonstrated that the consumption of soy protein decreases LDL-cholesterol, improves insulin sensitivity and attenuates body weight gain. Also, soy protein consumption can modify the gut microbiota, however it has not been established whether the changes in gut microbiota are in part responsible of the health effects of soy protein. Thus, the aim of the present study was to understand whether the metabolic effects of soy protein are reduced by the use of an antibiotic treatment. Methods Rats were fed for 16 weeks with one of the 4 experimental diets: 1) Casein control diet (C), 2) Soy protein diet (S), 3) C high-fat diet, and 4) S high-fat diet. Each group was sub-divided at the end of the 16 weeks in 2 groups. One subgroup continue with the same diet, and the other received the antibiotic treatment (Ampicillin/Neomycin) for 4 weeks. During the study body weight, food intake, body composition, energy expenditure and glucose tolerance were measured. Fecal samples were collected before and after the antibiotic treatment to determine the gut microbiota using the Illumina platform. At the end of the study blood samples were obtained to measure several biochemical variables. Also, liver and adipose tissue samples were obtained to assess the abundance of mRNA and proteins involved in lipid, glucose and thermogenesis. Results Rats fed S or S high fat diet had significant lower body weight gain, body fat, energy expenditure, glucose tolerance, blood lipids, increased expression of thermogenic genes and decreased serum lipopolisacharide than the control or high fat groups fed C diets. The antibiotic treatment abolished the health benefits observed in rats fed the S diets, particularly energy expenditure and weight gain. These changes were associated with changes in the gut microbiota, since S consumption increased the abundance of the Akkermansia and Bifidobacterium genus. This effect on the gut microbiota was prevented by the antibiotic treatment and rats developed metabolic endotoxemia. Finally, the antibiotic treatment reduced the expression of thermogenic genes, particularly in rats fed S high fat diet. Conclusions This study indicates that the beneficial effects of soy protein consumption on health are significantly dependent on the gut microbiota. Funding Sources CONACYT, INCMNSZ.

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