scholarly journals Comparing the metabolic fates of BALB/c mice maintained on cafeteria-style diets with differential nutritive values

2018 ◽  
Author(s):  
Muhammad Zaid ◽  
Fatima Ameer ◽  
Ayesha Ali ◽  
Zunaira Shoukat ◽  
Rida Rashid ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Dietary Intervention ◽  
Body Weight Gain ◽  
Plasma Lipid ◽  
Chow Diet ◽  
Food Items ◽  
Gain Rate ◽  
Weight Gain Rate ◽  
Diet Model

AbstractCafeteria (CAF) diet-fed rodents are shown to provide a robust model of metabolic syndrome and human obesity. The carbohydrate/fat-rich food-items provided to the CAF-diet-model more closely approximate the ultra-processed human diet. However, most of the previous studies applied the commercially available rodent chow-diet for the comparative analyses and labeled it as a healthy-diet. The presented work aims to extend the knowledge on CAF-diet model by exposing the mice to human foods with different nutritional values. Our major goal was to study the metabolic fates of mice maintained on human food-items, which depending upon on their macronutrient compositions are categorized as healthy or unhealthy. BALB/c mice were randomly allocated to one of the three dietary intervention groups, standard chow diet; high-sugar/high-fat-cafeteria (HSHF-CAF) diet; or low-sugar/low-fat-cafeteria (LSLF-CAF) diet, for 5 weeks. The differences in multiple metabolic parameters (including food-/energy /macronutrient-intake, body-weight gain rate, organ-to-body weight ratios, plasma lipid profiles, adipocyte physiology, lipid deposition in metabolic tissues and ectopic fat storage in heart and kidney) were compared among the three intervention groups. We did not observe hyperphagia in mice maintained on CAF-diets. Nonetheless, the CAF-diet-fed mice displayed increased weight-gain-rate, adiposity, and adipocyte hypertrophy when compared to the chow-fed mice. However, the mice maintained on the two cafeteria-style diets displayed similar metabolic profiles, with HSHF-CAF-group displaying slightly higher weight-gain-rate. The HSHF-CAF-and LSLF-CAF-diet induced comparable adiposity in BALB/c mice. Further studies, with longer dietary intervention periods, are required to elucidate the effects of differential CAF-diets on the metabolic health of mice.

Body weight gain rate in patients with Parkinson's disease and deep brain stimulation

2003 ◽  
Vol 18 (11) ◽  
pp. 1337-1340 ◽  
Author(s):  
Michela Barichella ◽  
Agnieszka M. Marczewska ◽  
Claudio Mariani ◽  
Andrea Landi ◽  
Antonella Vairo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Body Weight ◽  
Weight Gain ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Body Weight Gain ◽  
Gain Rate ◽  
Weight Gain Rate ◽  
Deep Brain

scholarly journals Effect of melatonin different time administration on the development of diet-induced obesity in rats

2017 ◽  
Vol 23 (2) ◽  
pp. 20-27 ◽  
Author(s):  
O. Kalmykova ◽  
A. Pustovalov ◽  
I. Vareniuk ◽  
M. Dzerzhynsky
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Weight Changes ◽  
Body Weight Changes ◽  
Evening Dose ◽  
Diet Induced Obesity ◽  
Time Treatment ◽  
Gain Rate ◽  
Weight Gain Rate

In recent years much attention has been paid for study of the melatonin use possibilities for improving obesity comorbidities. The aim of our study was to determine the influence of melatonin different time treatment on body weight changes of dietinduced obesity in rats. The administration by gavage of melatonin in dose 30 mg/kg for 7 weeks had the potential to decrease visceral fat weight, Lee index (both after morning and evening treatment) and body weight gain rate (only after evening dose).

scholarly journals Gut microbiota in obesity and metabolic disorders

2010 ◽  
Vol 69 (3) ◽  
pp. 434-441 ◽  
Author(s):  
Yolanda Sanz ◽  
Arlette Santacruz ◽  
Paola Gauffin
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Gut Microbiota ◽  
Metabolic Disorders ◽  
Dietary Intervention ◽  
Body Weight Gain ◽  
Human Subjects ◽  
Inflammatory Factors ◽  
Public Health Issue ◽  
Immune Functions

Obesity is a major public health issue as it is causally related to several chronic disorders, including type-2 diabetes, CVD and cancer. Novel research shows that the gut microbiota is involved in obesity and metabolic disorders, revealing that obese animal and human subjects have alterations in the composition of the gut microbiota compared to their lean counterparts. Moreover, transplantation of the microbiota of either obese or lean mice influences body weight in the germ-free recipient mice, suggesting that the gut ecosystem is a relevant target for weight management. Indigenous gut microbes may regulate body weight by influencing the host's metabolic, neuroendocrine and immune functions. The intestinal microbiota, as a whole, provides additional metabolic functions and regulates the host's gene expression, improving the ability to extract and store energy from the diet and contributing to body-weight gain. Imbalances in the gut microbiota and increases in plasma lipopolysaccharide may also act as inflammatory factors related to the development of atherosclerosis, insulin resistance and body-weight gain. In contrast, specific probiotics, prebiotics and related metabolites might exert beneficial effects on lipid and glucose metabolism, the production of satiety peptides and the inflammatory tone related to obesity and associated metabolic disorders. This knowledge is contributing to our understanding of how environmental factors influence obesity and associated diseases, providing new opportunities to design improved dietary intervention strategies to manage these disorders.

scholarly journals Effect of nicotine on body composition in mice

2011 ◽  
Vol 212 (3) ◽  
pp. 317-326 ◽  
Author(s):  
Michael Mangubat ◽  
Kabirullah Lutfy ◽  
Martin L Lee ◽  
Laura Pulido ◽  
David Stout ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Partial Agonist ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
Fat Distribution ◽  
Abdominal Fat ◽  
Chow Diet ◽  
Fat Composition

Nicotine induces weight loss in both humans and rodents consuming a regular diet; however, the effect of nicotine on body weight and fat composition in rodents consuming a high-fat diet (HFD) has not been well studied. Thus, this study examined the effect of nicotine vs saline on body weight and fat composition in mice fed with either an HFD (62% of kcal from fat) or a standard normal chow diet (NCD) for 7 weeks. Nicotine dose dependently reduced body weight gain in mice that consumed both diets, but this effect was significantly greater in mice on the HFD. Caloric intake was decreased in nicotine-treated mice. Estimates of energy intake suggested that decreased caloric intake accounted for all the reduced weight gain in mice on an NCD and 66% of the reduced weight gain on an HFD. Computed tomography analysis for fat distribution demonstrated that nicotine was effective in reducing abdominal fat in mice that consumed the HFD, with nicotine treatment leading to lower visceral fat. The effect of nicotine on weight loss in mice on an HFD was completely blocked by mecamylamine, a nonselective nicotinic acetylcholine receptor (nAChR) antagonist, but only partially blocked by the α4β2 nAChR partial agonist/antagonist, varenicline. We conclude that nicotine is effective in preventing HFD-induced weight gain and abdominal fat accumulation.

Effects of combined glucocorticoid/mineralocorticoid receptor modulation (CORT118335) on energy balance, adiposity, and lipid metabolism in male rats

2019 ◽  
Vol 317 (2) ◽  
pp. E337-E349
Author(s):  
Elizabeth T. Nguyen ◽  
Sarah Berman ◽  
Joshua Streicher ◽  
Christina M. Estrada ◽  
Jody L. Caldwell ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
The Body ◽  
Male Rats ◽  
Chow Diet ◽  
High Fat ◽  
Receptor Modulation

Psychological stress and excess glucocorticoids are associated with metabolic and cardiovascular diseases. Glucocorticoids act primarily through mineralocorticoid (MR) and glucocorticoid receptors (GR), and compounds modulating these receptors show promise in mitigating metabolic and cardiovascular-related phenotypes. CORT118335 (GR/MR modulator) prevents high-fat diet-induced weight gain and adiposity in mice, but the ability of this compound to reverse obesity-related symptoms is unknown. Adult male rats were subcutaneously administered CORT118335 (3, 10, or 30 mg/kg) or vehicle once daily. A 5-day treatment with CORT118335 at 30 mg/kg induced weight loss in rats fed a chow diet by decreasing food intake. However, lower doses of the compound attenuated body weight gain primarily because of decreased calorific efficiency, as there were no significant differences in food intake compared with vehicle. Notably, the body weight effects of CORT118335 persisted during a 2-wk treatment hiatus, suggesting prolonged effects of the compound. To our knowledge, we are the first to demonstrate a sustained effect of combined GR/MR modulation on body weight gain. These findings suggest that CORT118335 may have long-lasting effects, likely due to GR/MR-induced transcriptional changes. Prolonged (18 days) treatment of CORT118335 (10 mg/kg) reversed body weight gain and adiposity in animals fed a high-fat diet for 13 wk. Surprisingly, this occurred despite a worsening of the lipid profile and glucose homeostasis as well as a disrupted diurnal corticosterone rhythm, suggesting GR agonistic effects in the periphery. We conclude that species and tissue-specific targeting may result in promising leads for exploiting the metabolically beneficial aspects of GR/MR modulation.

scholarly journals Dietary Shiitake Mushroom (Lentinus edodes) Prevents Fat Deposition and Lowers Triglyceride in Rats Fed a High-Fat Diet

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
D. Handayani ◽  
J. Chen ◽  
B. J. Meyer ◽  
X. F. Huang
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Plasma Lipid ◽  
Fat Deposition ◽  
Shiitake Mushroom ◽  
High Fat ◽  
Plasma Triacylglycerol ◽  
Total Fat

High-fat diet (HFD) induces obesity. This study examined the effects of Shiitake mushroom on the prevention of alterations of plasma lipid profiles, fat deposition, energy efficiency, and body fat index induced by HFD. Rats were given a low, medium, and high (7, 20, 60 g/kg = LD-M, MD-M, HD-M) Shiitake mushroom powder in their high-fat (50% in kcal) diets for 6 weeks. The results showed that the rats on the HD-M diet had the lowest body weight gain compared to MD-M and LD-M groups (P<0.05). The total fat deposition was significantly lower (−35%,P<0.05) in rats fed an HD-M diet than that of HFD group. Interestingly, plasma triacylglycerol (TAG) level was significantly lower (−55%,P<0.05) in rats on HD-M than HFD. This study also revealed the existence of negative correlations between the amount of Shiitake mushroom supplementation and body weight gain, plasma TAG, and total fat masses.

Acutely reduced locomotor activity is a major contributor to Western diet-induced obesity in mice

2008 ◽  
Vol 294 (2) ◽  
pp. E251-E260 ◽  
Author(s):  
Mikael Bjursell ◽  
Anna-Karin Gerdin ◽  
Christopher J. Lelliott ◽  
Emil Egecioglu ◽  
Anders Elmgren ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Locomotor Activity ◽  
Body Temperature ◽  
Energy Intake ◽  
Body Weight Gain ◽  
Western Diet ◽  
Chow Diet ◽  
Brown Adipose ◽  
Obesity In Mice

The aim of the present study was to investigate the short- and long-term effects of a high-fat Western diet (WD) on intake, storage, expenditure, and fecal loss of energy as well as effects on locomotor activity and thermogenesis. WD for only 24 h resulted in a marked physiological shift in energy homeostasis, including increased body weight gain, body fat, and energy expenditure (EE) but an acutely lowered locomotor activity. The acute reduction in locomotor activity was observed after only 3–5 h on WD. The energy intake and energy absorption were increased during the first 24 h, lower after 72 h, and normalized between 7 and 14 days on WD compared with mice given chow diet. Core body temperature and EE was increased between 48 and 72 h but normalized after 21 days on WD. These changes paralleled plasma T3 levels and uncoupling protein-1 expression in brown adipose tissue. After 21 days of WD, energy intake and absorption, EE, and body temperature were normalized. In contrast, the locomotor activity was reduced and body weight gain was increased over the entire 21-day study period on WD. Calculations based on the correlation between locomotor activity and EE in 2-h intervals at days 21–23 indicated that a large portion of the higher body weight gain in the WD group could be attributed to the reduced locomotor activity. In summary, an acute and persisting decrease in locomotor activity is most important for the effect of WD on body weight gain and obesity in mice.

scholarly journals Evidence That Diet-Induced Hyperleptinemia, but Not Hypothalamic Gliosis, Causes Ghrelin Resistance in NPY/AgRP Neurons of Male Mice

Endocrinology ◽  
2014 ◽  
Vol 155 (7) ◽  
pp. 2411-2422 ◽  
Author(s):  
Dana I. Briggs ◽  
Sarah H. Lockie ◽  
Jonas Benzler ◽  
Qunli Wu ◽  
Romana Stark ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Time Course ◽  
Body Weight Gain ◽  
Calorie Intake ◽  
Chow Diet ◽  
Action Potential Firing ◽  
Whole Cell Patch Clamp ◽  
Potential Firing ◽  
Patch Clamp Electrophysiology

High-fat diet (HFD) feeding causes ghrelin resistance in arcuate neuropeptide Y (NPY)/Agouti-related peptide neurons. In the current study, we investigated the time course over which this occurs and the mechanisms responsible for ghrelin resistance. After 3 weeks of HFD feeding, neither peripheral nor central ghrelin increased food intake and or activated NPY neurons as demonstrated by a lack of Fos immunoreactivity or whole-cell patch-clamp electrophysiology. Pair-feeding studies that matched HFD calorie intake with chow calorie intake show that HFD exposure does not cause ghrelin resistance independent of body weight gain. We observed increased plasma leptin in mice fed a HFD for 3 weeks and show that leptin-deficient obese ob/ob mice are still ghrelin sensitive but become ghrelin resistant when central leptin is coadministered. Moreover, ob/ob mice fed a HFD for 3 weeks remain ghrelin sensitive, and the ability of ghrelin to induce action potential firing in NPY neurons was blocked by leptin. We also examined hypothalamic gliosis in mice fed a chow diet or HFD, as well as in ob/ob mice fed a chow diet or HFD and lean controls. HFD-fed mice exhibited increased glial fibrillary acidic protein–positive cells compared with chow-fed mice, suggesting that hypothalamic gliosis may underlie ghrelin resistance. However, we also observed an increase in hypothalamic gliosis in ob/ob mice fed a HFD compared with chow-fed ob/ob and lean control mice. Because ob/ob mice fed a HFD remain ghrelin sensitive, our results suggest that hypothalamic gliosis does not underlie ghrelin resistance. Further, pair-feeding a HFD to match the calorie intake of chow-fed controls did not increase body weight gain or cause central ghrelin resistance; thus, our evidence suggests that diet-induced hyperleptinemia, rather than diet-induced hypothalamic gliosis or HFD exposure, causes ghrelin resistance.

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