scholarly journals Behavioral and Metabolic Effects of a Calorie-Restricted Cafeteria Diet and Oleuropein Supplementation in Obese Male Rats

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4474
Author(s):  
Alex Subias-Gusils ◽  
Adam Álvarez-Monell ◽  
Noemí Boqué ◽  
Antoni Caimari ◽  
Josep M. Del Bas ◽  
...  
Keyword(s):  
Body Weight ◽  
Dietary Intervention ◽  
Body Weight Gain ◽  
High Energy ◽  
Sweet Taste ◽  
Cafeteria Diet ◽  
Metabolic Effects ◽  
Male Rats ◽  
Sucrose Intake ◽  
Obese Rats

Diet-induced obesity models are widely used to investigate dietary interventions for treating obesity. This study was aimed to test whether a dietary intervention based on a calorie-restricted cafeteria diet (CAF-R) and a polyphenolic compound (Oleuropein, OLE) supplementation modified sucrose intake, preference, and taste reactivity in cafeteria diet (CAF)-induced obese rats. CAF diet consists of high-energy, highly palatable human foods. Male rats fed standard chow (STD) or CAF diet were compared with obese rats fed CAF-R diet, alone or supplemented with an olive tree leaves extract (25 mg/kg*day) containing a 20.1% of OLE (CAF-RO). Biometric, food consumption, and serum parameters were measured. CAF diet increased body weight, food and energy consumption and obesity-associated metabolic parameters. CAF-R and CAF-RO diets significantly attenuated body weight gain and BMI, diminished food and energy intake and improved biochemical parameters such as triacylglycerides and insulin resistance which did not differ between CAF-RO and STD groups. The three cafeteria groups diminished sucrose intake and preference compared to STD group. CAF-RO also diminished the hedonic responses for the high sucrose concentrations compared with the other groups. These results indicate that CAF-R diet may be an efficient strategy to restore obesity-associated alterations, whilst OLE supplementation seems to have an additional beneficial effect on sweet taste function.

PYY(3–36) reduces food intake and body weight and improves insulin sensitivity in rodent models of diet-induced obesity

2006 ◽  
Vol 291 (2) ◽  
pp. R367-R375 ◽  
Author(s):  
Niels Vrang ◽  
Andreas Nygaard Madsen ◽  
Mads Tang-Christensen ◽  
Gitte Hansen ◽  
Philip Just Larsen
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Peptide Yy ◽  
Body Weight Gain ◽  
Subcutaneous Administration ◽  
Treated Group ◽  
Metabolic Effects ◽  
Male Rats ◽  
Reduced Body ◽  
Gut Hormone

The gut hormone peptide YY (PYY) was recently proposed to comprise an endogenous satiety factor. We have studied acute anorectic functions of PYY(3–36) in mice and rats, as well as metabolic effects of chronic PYY(3–36) administration to diet-induced obese (DIO) mice and rats. A single intraperitoneal injection of PYY(3–36) inhibited food intake in mice, but not in rats. We next investigated the effects of increasing doses (100, 300, and 1,000 μg·kg−1·day−1) of PYY(3–36) administered subcutaneously via osmotic minipumps on food intake and body weight in DIO C57BL/6J mice. Whereas only the highest dose (1,000 μg·kg−1·day−1) of PYY(3–36) significantly reduced food intake over the first 3 days, body weight gain was dose dependently reduced, and on day 28 the group treated with 1,000 μg·kg−1·day−1 PYY(3–36) weighed ∼10% less than the vehicle-treated group. Mesenteric, epididymal, retroperitoneal, and inguinal fat pad weight was dose dependently reduced. Subcutaneous administration of PYY(3–36) (250 and 1,000 μg·kg−1·day−1) for 28 days reduced body weight and improved glycemic control in glucose-intolerant DIO rats. Neither 250 nor 1,000 μg/kg PYY(3–36) elicited a conditioned taste aversion in male rats.

Metabolic effects of chronic infusions of epinephrine and norepinephrine in rats

1986 ◽  
Vol 250 (5) ◽  
pp. E518-E522 ◽  
Author(s):  
R. Racotta ◽  
L. Ramirez-Altamirano ◽  
E. Velasco-Delgado
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Chronic Administration ◽  
Metabolic Effects ◽  
Male Rats ◽  
Epinephrine Infusion ◽  
Calculated Dose

Chronic infusions of epinephrine, norepinephrine, or vehicle were performed in adult male rats by means of subcutaneous implanted osmotic minipumps (ALZET). The calculated dose was 180 ng/min during 7-8 days. Daily food intake and body weight were measured during this period and also 7 days before and 5 days after it. During the period of infusion, norepinephrine stopped body weight gain while epinephrine-infused rats gained weight at the same rate as controls. Once the infusion period was finished, epinephrine-infused rats gained more weight than controls, while norepinephrine-infused rats just returned to the slope of weight gain of the controls. In no group did food intake change. In a second experiment, similar infusions were carried out in other rats on the same schedule; body temperature, glycemia, and serum insulin and triiodothyronine were measured. Epinephrine infusion significantly elevated glycemia and triiodothyronine, whereas norepinephrine infusion increased temperature and serum insulin. The results obtained by chronic administration of the catecholamines support the concept of a disassociation of adrenomedullary and sympathetic nervous system metabolic effects.

scholarly journals Neonatal nutritional programming impairs adiponectin effects on energy homeostasis in adult life of male rats

2018 ◽  
Vol 315 (1) ◽  
pp. E29-E37 ◽  
Author(s):  
Mariana Peduti Halah ◽  
Paula Beatriz Marangon ◽  
Jose Antunes-Rodrigues ◽  
Lucila L. K. Elias
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
White Adipose Tissue ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
Adult Life ◽  
Male Rats ◽  
Nutritional Programming

Neonatal nutritional changes induce long-lasting effects on energy homeostasis. Adiponectin influences food intake and body weight. The aim of this study was to investigate the effects of neonatal nutritional programming on the central stimulation of adiponectin. Male Wistar rats were divided on postnatal (PN) day 3 in litters of 3 (small litter, SL), 10 (normal litter, NL), or 16 pups/dam (large litter, LL). We assessed body weight gain for 60 days, adiponectin concentration, and white adipose tissue weight. We examined the response of SL, NL, and LL rats on body weight gain, food intake, oxygen consumption (V̇o2), respiratory exchange ratio (RER), calorimetry, locomotor activity, phosphorylated-AMP-activated protein kinase (AMPK) expression in the hypothalamus, and uncoupling protein (UCP)-1 in the brown adipose tissue after central stimulus with adiponectin. After weaning, SL rats maintained higher body weight gain despite similar food intake compared with NL rats. LL rats showed lower body weight at weaning, with a catch up afterward and higher food intake. Both LL and SL groups had decreased plasma concentrations of adiponectin at PN60. SL rats had increased white adipose tissue. Central injection of adiponectin decreased body weight and food intake and increased V̇o2, RER, calorimetry, p-AMPK and UCP- 1 expression in NL rats, but it had no effect on SL and LL rats, compared with the respective vehicle groups. In conclusion, neonatal under- and overfeeding induced an increase in body weight gain in juvenile and early adult life. Unresponsiveness to central effects of adiponectin contributes to the imbalance of the energy homeostasis in adult life induced by neonatal nutritional programming.

scholarly journals POTENTIAL OF DUNALIELLA SALINA MICROALGAE TO AMELIORATE HIGH-FAT DIET‑INDUCED OBESITY IN ANIMALS’ RODENT

2018 ◽  
Vol 11 (3) ◽  
pp. 312 ◽  
Author(s):  
Farouk K El-baz ◽  
Hanan F Aly
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Dunaliella Salina ◽  
Body Weight Gain ◽  
Ethanolic Extract ◽  
High Fat ◽  
Related Complication ◽  
Standard Drug ◽  
Reduced Body ◽  
Obese Rats

 Objective: This study was carried out to investigate the potential of Dunaliella salina microalgae to ameliorate obesity induced by high-fat diet (HFD) in male Wistar rats.Methods: Fifty rats weighing 150–160 g were fed HFD for 12 weeks. The rats were randomly divided into five groups of ten rats each. Obese rats were orally administered D. salina ethanolic extract (150 mg/Kg body weight), and orlistat as standard drug (12 mg/Kg body weight), for 6 weeks.Results: Treatment of obese rats with both D. salina and orlistat had a significant effect in reducing body and liver weights as well as visceral fat, inhibiting pancreatic lipase activity, decreased lipid profile, and increased fecal fat and ameliorating liver function enzymes activity, insulin, blood glucose, and leptin levels. Besides, food intake was insignificantly increased as a result of D. salina and orlistat treatments compared with normal control rats.Conclusion: It could be concluded that D. salina rich in β-carotene significantly reduced body weight gain and ameliorated several metabolic pathways implicated in obesity and its related complication. Hence, further intensive study must be carried out to formulate D. Salina extracts to apply as a promising natural anti-obesity nutraceutical drug.

scholarly journals Effects of fructose and glucose on plasma leptin, insulin, and insulin resistance in lean and VMH-lesioned obese rats

2000 ◽  
Vol 278 (4) ◽  
pp. E677-E683 ◽  
Author(s):  
Asako Suga ◽  
Tsutomu Hirano ◽  
Haruaki Kageyama ◽  
Toshimasa Osaka ◽  
Yoshio Namba ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Body Weight Gain ◽  
Intravenous Glucose Tolerance Test ◽  
Fat Pad ◽  
Intravenous Glucose ◽  
Dietary Fructose ◽  
Obese Rats ◽  
Normal Chow ◽  
Plasma Leptin

To determine the influence of dietary fructose and glucose on circulating leptin levels in lean and obese rats, plasma leptin concentrations were measured in ventromedial hypothalamic (VMH)-lesioned obese and sham-operated lean rats fed either normal chow or fructose- or glucose-enriched diets (60% by calories) for 2 wk. Insulin resistance was evaluated by the steady-state plasma glucose method and intravenous glucose tolerance test. In lean rats, glucose-enriched diet significantly increased plasma leptin with enlarged parametrial fat pad, whereas neither leptin nor fat-pad weight was altered by fructose. Two weeks after the lesions, the rats fed normal chow had marked greater body weight gain, enlarged fat pads, and higher insulin and leptin compared with sham-operated rats. Despite a marked adiposity and hyperinsulinemia, insulin resistance was not increased in VMH-lesioned rats. Fructose brought about substantial insulin resistance and hyperinsulinemia in both lean and obese rats, whereas glucose led to rather enhanced insulin sensitivity. Leptin, body weight, and fat pad were not significantly altered by either fructose or glucose in the obese rats. These results suggest that dietary glucose stimulates leptin production by increasing adipose tissue or stimulating glucose metabolism in lean rats. Hyperleptinemia in VMH-lesioned rats is associated with both increased adiposity and hyperinsulinemia but not with insulin resistance. Dietary fructose does not alter leptin levels, although this sugar brings about hyperinsulinemia and insulin resistance, suggesting that hyperinsulinemia compensated for insulin resistance does not stimulate leptin production.

scholarly journals Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-α

2007 ◽  
Vol 97 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Patricia Pérez-Matute ◽  
Nerea Pérez-Echarri ◽  
J. Alfredo Martínez ◽  
Amelia Marti ◽  
María J. Moreno-Aliaga
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Control Diet ◽  
Cafeteria Diet ◽  
High Fat ◽  
Beneficial Effects

n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0·09), a decrease in food intake (P < 0·01) and an increase in leptin production (P < 0·05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0·05) which could be secondary to the inhibition of the adipogenic transcription factor PPARγ gene expression (P < 0·001), and also to the increase in apoptosis (P < 0·05) found in rats fed with a control diet. TNFα gene expression was significantly increased (P < 0·05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0·01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFα and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.

scholarly journals Losartan prevents body weight gain in diet induced obese rats

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Pauline M Smith ◽  
Charles C.T. Hindmarch ◽  
David Murphy ◽  
Alastair V. Ferguson
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Obese Rats

Bimatoprost promotes satiety and attenuates body weight in rats fed standard or obesity-promoting diets.

2020 ◽  
Author(s):  
Clayton Spada ◽  
Chau Vu ◽  
Iona Raymond ◽  
Warren Tong ◽  
Chia-Lin Chuang ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Gastric Emptying ◽  
Food Intake ◽  
Visceral Fat ◽  
Body Weight Gain ◽  
Metabolic Effects ◽  
Sprague Dawley ◽  
Hormone Levels ◽  
Gut Hormone

Abstract Background Bimatoprost negatively regulates adipogenesis in vitro and likely participates in a negative feedback loop on anandamide-induced adipogenesis. Here, we investigate the broader metabolic effects of bimatoprost action in vivo in rats under both normal state and obesity-inducing conditions. Methods Male Sprague Dawley rats were a fed standard chow (SC) diet in conjunction with dermally applied bimatoprost treatment for a period of 9–10 weeks. Body weight gain, energy expenditure, food intake, and hormones associated with satiety were measured. Gastric emptying was also separately evaluated. In obesity-promoting diet studies, rats were fed a cafeteria diet (CAF) and gross weight, fat accumulation in SQ, visceral fat and liver was evaluated together with standard serum chemistry. Results Chronic bimatoprost administration attenuated weight gain in rats fed either standard or obesity-promoting diets over a 9–10 weeks. Bimatoprost increased satiety as measured by decreased food intake, gastric emptying and circulating gut hormone levels. Additionally, SQ and visceral fat mass was distinctly affected by treatment. Bimatoprost increased satiety as measured by decreased food intake, gastric emptying and circulating gut hormone levels. Conclusions These findings suggest that bimatoprost (and possibly prostamide F2α) regulates energy homeostasis through actions on dietary intake. These actions likely counteract the metabolic actions of anandamide through the endocannabinoid system potentially revealing a new pathway that could be exploited for therapeutic development.

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