Effect of Bergenia crassifolia L. extracts on weight gain and feeding behavior of rats with high-caloric diet-induced obesity

Background: The Rho-activated kinases (ROCK1 and ROCK2) are serine threonine kinases that are ubiquitously expressed with higher levels of ROCK2 compared to ROCK1 in adipocytes. Recent studies suggest that ROCK2 may be an important regulator of energy metabolism and obesity. However, its role in adipocyte development and function is unknown. Methods and Result: To determine the role of ROCK2 in adipocyte development and obesity, we generated adipocyte-specific deletion (ROCK2 adipoQ-/- ) and overexpression (CA-ROCK adipoQ+/+ ) of ROCK2 in mice. Compared to control mice, CA-ROCK adipoQ+/+ mice exhibited increased browning of inguinal white adipose tissue (iWAT). Indeed, immunohistochemical staining of iWAT in CA-ROCK adipoQ+/+ mice showed that UCP1 was upregulated. Furthermore, CA-ROCK adipoQ+/+ mice on high fat diet were resistant to weight gain and obesity for up to 18 weeks. This is in contrast to ROCK2 adipoQ-/- mice, which developed more weight gain or obesity than control mice. To determine the physiological effects of ROCK2 on browning of iWAT, control and ROCK2 adipoQ-/- mice were exposed to 4°C for 1 week. In control mice, cold exposure increased ROCK2 activity and lead to browning of iWAT. However, the iWAT in ROCK2 adipoQ-/- mice failed to undergo browning. Analysis of gene expression in iWAT demonstrated increased UCP1 and mitochondria proteins in control but not ROCK2 adipoQ-/- mice. Thermal imaging revealed that ROCK2 adipoQ-/- mice were unable to maintain basal body temperature after prolonged cold exposure. In contrast, the heat map of the CA-ROCK adipoQ+/+ mice showed an elevation of body temperature, particularly in areas of iWAT as compared to that of control littermates. Conclusions: ROCK2 mediates the “browning” of white adipocytes and prevents the development of obesity through increased thermogenesis. These findings suggest that the activation of ROCK2 in adipocytes may have therapeutic benefits in preventing diet-induced obesity.

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Extract of Irish potatoes (Solanum tuberosumL.) decreases body weight gain and adiposity and improves glucose control in the mouse model of diet-induced obesity

Molecular Nutrition & Food Research ◽

10.1002/mnfr.201400013 ◽

2014 ◽

Vol 58 (11) ◽

pp. 2235-2238 ◽

Cited By ~ 12

Author(s):

Stan Kubow ◽

Luc Hobson ◽

Michèle M. Iskandar ◽

Kebba Sabally ◽

Danielle J. Donnelly ◽

...

Keyword(s):

Body Weight ◽

Weight Gain ◽

Mouse Model ◽

Glucose Control ◽

Body Weight Gain ◽

Diet Induced Obesity

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Effects of Melatonin on Lipid Metabolism and Circulating Irisin in Sprague-Dawley Rats with Diet-Induced Obesity

Molecules ◽

10.3390/molecules25153329 ◽

2020 ◽

Vol 25 (15) ◽

pp. 3329

Author(s):

Yu-Tang Tung ◽

Pei-Chin Chiang ◽

Ya-Ling Chen ◽

Yi-Wen Chien

Keyword(s):

Weight Gain ◽

Total Cholesterol ◽

Vehicle Control ◽

Serum Total Cholesterol ◽

Sprague Dawley ◽

High Fat ◽

Melatonin Treatment ◽

Diet Induced Obesity ◽

Sprague Dawley Rats ◽

Cholesterol Excretion

Melatonin, a pivotal photoperiodic signal transducer, may work as a brown-fat inducer that regulates energy balance. Our study aimed to investigate the effects of melatonin treatment on the body fat accumulation, lipid profiles, and circulating irisin of rats with high-fat diet-induced obesity (DIO). Methods: 30 male Sprague-Dawley rats were divided into five groups and treated for 8 weeks: vehicle control (VC), positive control (PC), MEL10 (10 mg melatonin/kg body weight (BW)), MEL20 (20 mg/kg BW), and MEL50 (50 mg/kg BW). The vehicle control group was fed a control diet, and the other groups were fed a high-fat and high-calorie diet for 8 weeks to induce obesity before the melatonin treatment began. Melatonin reduced weight gain without affecting the food intake, reduced the serum total cholesterol level, enhanced the fecal cholesterol excretion, and increased the circulating irisin level. Melatonin downregulated the fibronectin type III domain containing 5 (FNDC5) and lipoprotein lipase (LPL) mRNA expressions of inguinal white adipose tissue (iWAT) and induced the browning of iWAT in both the MEL10 and MEL20 groups. Conclusion: Chronic continuous melatonin administration in drinking water reduced weight gain and the serum total cholesterol levels. Additionally, it enhanced the circulating irisin, which promoted brite/beige adipocyte recruitment together with cholesterol excretion and contributed to an anti-obesity effect.

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Comparison of the effects of microinjections of angiotensin II and bradykinin into the lateral ventricles and their instillation into the conjunctiva on feeding behavior of rats

Bulletin of Experimental Biology and Medicine ◽

10.1007/bf00839608 ◽

1986 ◽

Vol 101 (6) ◽

pp. 792-795

Author(s):

L. F. Kelesheva

Keyword(s):

Angiotensin Ii ◽

Feeding Behavior ◽

Lateral Ventricles ◽

Behavior Of Rats

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Leptin resistance: a prediposing factor for diet-induced obesity

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.90669.2008 ◽

2009 ◽

Vol 296 (3) ◽

pp. R493-R500 ◽

Cited By ~ 124

Author(s):

Philip J. Scarpace ◽

Yi Zhang

Keyword(s):

Weight Gain ◽

Leptin Receptor ◽

Causative Factor ◽

Leptin Resistance ◽

Chow Diet ◽

High Fat ◽

Diet Induced Obesity ◽

Dietary Fructose ◽

Complex Chronic Disease ◽

Obesity Syndrome

Obesity is a resilient and complex chronic disease. One potential causative factor in the obesity syndrome is leptin resistance. Leptin behaves as a potent anorexic and energy-enhancing hormone in most young or lean animals, but its effects are diminished or lacking in the obese state associated with a normal genetic background. Emerging evidence suggests that leptin resistance predisposes the animal to exacerbated diet-induced obesity (DIO). Elevation of central leptin in young, lean rats induces a leptin resistance that precludes obesity on a chow diet but accelerates high-fat (HF)-induced obesity. Similarly, chronic dietary fructose consumption evokes a leptin resistance that causes obesity only upon HF exposure. Inherent central leptin insensitivity also contributes to dietary weight gain in certain obesity-prone rats. Conversely, aged, leptin-resistant animals are obese with continuous chow feeding and demonstrate aggravated obesity when challenged with an HF diet. Additionally, a submaximal central blockade with a leptin antagonist leads to obesity on both chow and HF diets, as is the case in rodents with leptin receptor deficiency of genetic origin. Despite the differences in the incidence of obesity on a chow diet, all of these forms of leptin resistance predispose rodents to aggravated HF-mediated obesity. Moreover, once leptin resistance takes hold, it aggravates DIO, and the leptin resistance and obesity compound one another, promoting a vicious cycle of escalating weight gain.

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Improved Insulin Resistance and Lipid Metabolism by Cinnamon Extract through Activation of Peroxisome Proliferator-Activated Receptors

PPAR Research ◽

10.1155/2008/581348 ◽

2008 ◽

Vol 2008 ◽

pp. 1-9 ◽

Cited By ~ 83

Author(s):

Xiaoyan Sheng ◽

Yuebo Zhang ◽

Zhenwei Gong ◽

Cheng Huang ◽

Ying Qin Zang

Keyword(s):

Insulin Resistance ◽

Target Genes ◽

Water Extract ◽

Food Preparation ◽

Peroxisome Proliferator ◽

Cinnamon Extract ◽

Diet Induced Obesity ◽

Peroxisome Proliferator Activated Receptors ◽

High Caloric Diet

Peroxisome proliferator-activated receptors (PPARs) are transcriptional factors involved in the regulation of insulin resistance and adipogenesis. Cinnamon, a widely used spice in food preparation and traditional antidiabetic remedy, is found to activate PPARγandα, resulting in improved insulin resistance, reduced fasted glucose, FFA, LDL-c, and AST levels in high-caloric diet-induced obesity (DIO) anddb/dbmice in its water extract form. In vitro studies demonstrate that cinnamon increases the expression of peroxisome proliferator-activated receptorsγandα(PPARγ/α) and their target genes such as LPL, CD36, GLUT4, and ACO in 3T3-L1 adipocyte. The transactivities of both full length and ligand-binding domain (LBD) of PPARγand PPARαare activated by cinnamon as evidenced by reporter gene assays. These data suggest that cinnamon in its water extract form can act as a dual activator of PPARγandα, and may be an alternative to PPARγactivator in managing obesity-related diabetes and hyperlipidemia.

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