Light intensity alters the effects of light-induced circadian disruption on glucose and lipid metabolism in mice

2021 ◽  
Author(s):  
Xiaojing Fan ◽  
Defu Chen ◽  
Ying Wang ◽  
Yizhou Tan ◽  
Hongyou Zhao ◽  
...  
Keyword(s):  
Body Weight ◽  
Light Intensity ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Circadian Disruption ◽  
Light Cycle ◽  
Jet Lag ◽  
Glucose And Lipid Metabolism ◽  
Insulin Tolerance ◽  
Potential Strategy

Circadian disruption induced by rotating light cycles has been linked to metabolic disorders. However, how the interaction of light intensity and light cycle affects metabolism under different diets remains to be explored. Eighty mice were first randomly stratified into the low- (LFD, n = 40) or high-fat diet (HFD, n = 40) groups. Each group was further randomly subdivided into four groups (n = 8-12 per group) in terms of different light intensities (lower [LI, 78 lx] or higher intensity [HI, 169 lx]) and light cycles (12 h light:12 h dark cycle or circadian-disrupting [CD] light cycle consisting of repeated 6-h light phase advancement). Body weight was measured weekly. At the end of the 16-week experiment, mice were sacrificed for serum and pathological analysis. Glucose and insulin tolerance tests were performed during the last 2 weeks. The CD cycle increased body weight gain, adipocyte area, glucose intolerance, and insulin resistance of LFD as well as HFD mice under HI but not LI condition. Moreover, the serum and hepatic triglyceride levels increased with LFD-HI treatment, regardless of light cycle. In addition, the CD cycle improved lipid and glucose metabolism under HFD-LI condition. In summary, the detrimental effects of the CD cycle on metabolism were alleviated under LI condition, especially in HFD mice. These results indicate that modulating light intensity is a potential strategy to prevent the negative metabolic consequences associated with jet lag or shift work.

scholarly journals Combination Treatment of Arazyme and Soy Leaf Extract Attenuates Hyperglycemia and Hepatic Steatosis in High-Fat Diet-Fed C57BL/6J Mice

Life ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 645
Author(s):  
Hwa Lee ◽  
Seona Cho ◽  
Anna Kang ◽  
Dong-Ha Shin ◽  
Ho-Yong Park ◽  
...  
Keyword(s):  
Body Weight ◽  
Bile Acid ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Lipid Synthesis ◽  
Therapeutic Effects ◽  
High Fat ◽  
Insulin Tolerance ◽  
Bile Acid Transporter

Arazyme and extracts of soy leaves (ESLs) are used as ingredients for functional foods; however, their combined administration has not been studied. This study assessed the combined effect of Arazyme and ESLs in high-fat-diet (HFD)-induced obese C57BL/6J mice fed 2 mg/kg Arazyme, 50 mg/kg ESLs, or a combination of 2 mg/kg Arazyme and 50 mg/kg ESLs by oral gavage for 13 weeks. Individually, Arazyme and ESLs had no effect on the HFD-induced phenotypes. The combination of Arazyme and ESLs significantly suppressed body weight gain, improved glucose and insulin tolerance, and suppressed hepatic steatosis by reducing lipid synthesis and enhancing lipid utilization gene expression. Furthermore, the combination significantly reduced HFD-induced plasma bile acid reabsorption by suppressing bile acid transporter expression, including the ATP biding cassette subfamily B member 11 (Abcb11), solute carrier family 10 member 1 (Slc10a1), Slc10a2, Slc51a, and Slc51b in the liver and gut. Moreover, the combination of Arazyme and ESLs significantly prevented HFD-induced islet compensation in the pancreas. These results suggest that the incorporation of Arazyme combined with ESLs reduces HFD-induced body weight, hyperglycemia, and hepatic steatosis by regulating liver–gut bile acid circulation in HFD-fed mice. This combination can markedly reduce treatment doses and enhance their therapeutic effects, thereby reducing therapeutic healthcare costs.

scholarly journals Chronic photoperiodic manipulation induced chronodisruption upregulates HSP60 during early pro-atherogenic remodeling in thoracic aorta of C57BL/6J mice

2021 ◽  
Vol 82 (1) ◽  
Author(s):  
Kavita Shirsath ◽  
Apeksha Joshi ◽  
Aliasgar Vohra ◽  
Ranjitsinh Devkar
Keyword(s):  
Body Weight ◽  
Thoracic Aorta ◽  
Serum Lipid ◽  
Body Weight Gain ◽  
Hdl Cholesterol ◽  
Circadian Disruption ◽  
Control Group ◽  
Chow Diet ◽  
Heat Shock Protein 60 ◽  
Lipid Parameters

Abstract Background Circadian disruption is often associated with aggravation of atherosclerosis; however, the pathophysiological mechanisms underlying atherogenic initiation in normolipidemic diet remains unclear. Most of the studies done for understanding circadian disruption induced atherosclerosis have been carried out in murine model of hyperlipidemia induced atherosclerosis. The present study investigates pro-atherogenic events in response to chronic photoperiodic manipulation induced chronodisruption (PMCD) in C57BL/6J mice fed with laboratory chow diet. Results The results were compared with atherogenic initiation induced by high fat high fructose (HFHF) diet. The combined effects of HFHF and PMCD on atherogenic initiation were also investigated for possible synergy of both variants. The HFHF and HFHF+PMCD groups recorded increments in body weight gains and serum lipid parameters (TC, TG, LDL-cholesterol, VLDL) and a decrement in HDL-cholesterol as compared to the control group. However, PMCD group recorded body weight gain similar to that of the control group, but the serum lipid parameters (TG and VLDL) were significantly elevated and the HDL levels were lowered. However, prominent hypertrophic remodeling, higher collagen deposition, and elastin derangement, along with endothelial dysfunction, its activation, and macrophage infiltration, were observed in thoracic aorta of all the three experimental groups. But the mRNA and immunoblots of heat shock protein 60 (HSP60) in thoracic aorta was found to be maximum in PMCD followed by HFHF and HFHF+PMCD groups. Conclusion Laboratory chow feeding coupled with photoperiodic manipulation mediated chronodisruption overexpress HSP60 that in turn plays a central role in PMCD mediated pro-atherogenic remodeling in thoracic aorta of C57BL/6J mice.

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 Tetrahydro iso-Alpha Acids from Hops Improve Glucose Homeostasis and Reduce Body Weight Gain and Metabolic Endotoxemia in High-Fat Diet-Fed Mice

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e33858 ◽  
Author(s):  
Amandine Everard ◽  
Lucie Geurts ◽  
Marie Van Roye ◽  
Nathalie M. Delzenne ◽  
Patrice D. Cani
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
High Fat ◽  
Reduce Body Weight ◽  
Metabolic Endotoxemia

scholarly journals Fish oil suppresses obesity more potently in lean mice than in diet-induced obese mice but ameliorates steatosis in such obese mice

2021 ◽  
Vol 85 (2) ◽  
pp. 421-429
Author(s):  
Sachiko Okue ◽  
Eimi Ishikawa ◽  
Ren Nakahara ◽  
Tsubasa Ito ◽  
Takumi Okura ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Fish Oil ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Uncoupling Protein ◽  
Liver Steatosis ◽  
Obese Mice ◽  
Food Efficiency ◽  
Lard Diet

ABSTRACT This study sought to clarify the antiobesity effects of fish oil (FO) in terms of prevention and amelioration. An isocaloric diet composed of lard or FO was given to lean C57BL/6J mice for the study of prevention and high-fat diet-induced obese (DIO) mice for the study of amelioration for 4 weeks. Body weight gain and food efficiency were potently suppressed by FO in lean mice compared to lard diet-fed mice. Uncoupling protein-1 (UCP-1) expression in inguinal white adipose tissue (WAT) was also significantly induced by FO in lean mice. FO also suppressed body weight gain and food efficiency in DIO mice but did not reduce body weight. FO ameliorated liver steatosis in DIO mice by mildly inducing UCP-1 in inguinal WAT. FO suppressed obesity more potently in lean mice than in DIO mice but ameliorated steatosis in the DIO mice.

scholarly journals Early Overnutrition Results in Early-Onset Arcuate Leptin Resistance and Increased Sensitivity to High-Fat Diet

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1598-1610 ◽  
Author(s):  
Maria M. Glavas ◽  
Melissa A. Kirigiti ◽  
Xiao Q. Xiao ◽  
Pablo J. Enriori ◽  
Sarah K. Fisher ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
High Fat Diet ◽  
Arcuate Nucleus ◽  
Leptin Resistance ◽  
Signal Transducer ◽  
High Fat ◽  
Insulin Tolerance ◽  
Obesity And Diabetes ◽  
Transcription 3

Childhood obesity increases the risk of adult obesity and diabetes, suggesting that early overnutrition permanently programs altered energy and glucose homeostasis. In the present studies, we used a mouse model to investigate whether early overnutrition increases susceptibility to obesity and insulin resistance in response to a high-fat diet (HFD). Litters from Swiss Webster dams were culled to three [chronic postnatal overnutrition (CPO)] or 10 (control) pups and then weaned onto standard chow at postnatal day (P) 23. At 6 wk of age, a subset of mice was placed on HFD, and glucose and insulin tolerance were examined at 16–17 wk of age. Leptin sensitivity was determined by hypothalamic phosphorylated signal transducer and activator of transcription-3 immunoreactivity at P16 and adulthood after ip leptin. CPO mice exhibited accelerated body weight gain and hyperleptinemia during the preweaning period but only a slightly heavier body weight and normal glucose tolerance in adulthood on standard chow diet. Importantly, CPO mice exhibited significant leptin resistance in the arcuate nucleus, demonstrated by reduced activation of phospho-signal transducer and activator of transcription-3, as early as P16 and throughout life, despite normalized leptin levels. In response to HFD, CPO but not control mice displayed insulin resistance in response to an insulin tolerance test. In conclusion, CPO mice exhibited early and persistent leptin resistance in the arcuate nucleus and, in response to HFD, rapid development of obesity and insulin resistance. These studies suggest that early overnutrition can permanently alter energy homeostasis and significantly increase susceptibility to obesity and insulin resistance.

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