scholarly journals Supplementation with Sea Vegetables Palmaria mollis and Undaria pinnatifida Exerts Metabolic Benefits in Diet-Induced Obesity in Mice

2020 ◽  
Vol 4 (5) ◽  
Author(s):  
Rufa L Mendez ◽  
Cristobal Miranda ◽  
Courtney R Armour ◽  
Thomas J Sharpton ◽  
Jan Frederik Stevens ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
High Fat Diet ◽  
Undaria Pinnatifida ◽  
Lipid Absorption ◽  
Health Improvement ◽  
High Fat ◽  
Metabolic Complications ◽  
Diet Induced Obesity ◽  
Sea Vegetables ◽  
Lipid Excretion

ABSTRACT Background Sea vegetables are rich sources of nutrients as well as bioactive components that are linked to metabolic health improvement. Algal polysaccharides improve satiety and modulate gut microbiota while proteins, peptides, and phenolic fractions exert anti-inflammatory, antioxidant, and antidiabetic effects. Objective We tested the hypothesis that dietary supplementation with either Pacific dulse (Palmaria mollis, red algae) or wakame (Undaria pinnatifida, brown algae) could remediate metabolic complications in high-fat diet-induced obesity. Methods Individually caged C57BL/6J mice (n = 8) were fed ad libitum with either a low-fat diet (LFD), 10% kcal fat; high-fat diet (HFD), 60% kcal fat; HFD + 5% (wt:wt) dulse (HFD + D); or HFD + 5% (wt:wt) wakame (HFD + W) for 8 weeks. Food intake and weight gain were monitored weekly. Glucose tolerance, hepatic lipids, fecal lipids, and plasma markers were evaluated, and the gut microbiome composition was assessed. Results Despite the tendency of higher food and caloric intake than the HFD (P = 0.04) group, the HFD + D group mice did not exhibit higher body weight, indicating lower food and caloric efficiency (P < 0.001). Sea vegetable supplementation reduced plasma monocyte chemotactic protein (MCP-1) (P < 0.001) and increased fecal lipid excretion (P < 0.001). Gut microbiome analysis showed that the HFD + D group had higher alpha-diversity than the HFD or LFD group, whereas beta-diversity analyses indicated that sea vegetable–supplemented HFD-fed mice (HFD + D and HFD + W groups) developed microbiome compositions more similar to those of the LFD-fed mice than those of the HFD-fed mice. Conclusion Sea vegetable supplementation showed protective effects against obesity-associated metabolic complications in C57BL/6J male mice by increasing lipid excretion, reducing systemic inflammatory marker, and mitigating gut microbiome alteration. While the obese phenotype development was not prevented, metabolic issues related to lipid absorption, inflammation, and gut microbial balance were improved, showing therapeutic promise and warranting eventual mechanistic elucidations.

scholarly journals Celastrol inhibits intestinal lipid absorption by reprofiling the gut microbiota to attenuate high-fat diet-induced obesity

iScience ◽  
2021 ◽  
Vol 24 (2) ◽  
pp. 102077
Author(s):  
Hu Hua ◽  
Yue Zhang ◽  
Fei Zhao ◽  
Ke Chen ◽  
Tong Wu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Lipid Absorption ◽  
High Fat ◽  
Diet Induced Obesity

Seabuckthorn polysaccharide ameliorates high-fat diet-induced obesity by gut microbiota-SCFAs-liver axis

2022 ◽  
Author(s):  
Ying Lan ◽  
Qingyang Sun ◽  
Zhiyuan Ma ◽  
Jing Peng ◽  
Mengqi Zhang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity

Obesity has been reported to be associated with gut microbiome dysbiosis. seabuckthorn fruits are traditionally used in Tibetan foods and medicines for thousands of years. Seabuckthorn polysaccharide (SP) is one...

scholarly journals Estradiol modulates gut microbiota in female ob/ob mice fed a high fat diet

2019 ◽  
Author(s):  
Kalpana D Acharya ◽  
Xing Gao ◽  
Elizabeth P Bless ◽  
Jun Chen ◽  
Marc J Tetel
Keyword(s):  
Weight Gain ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
High Fat ◽  
Diet Induced Obesity ◽  
The Family ◽  
Satiety Hormone ◽  
17Β Estradiol

AbstractEstrogens protect against diet-induced obesity in women and female rodents. In support of these anorectic effects, lack of estrogens in postmenopausal women is associated with weight gain, increasing their risk for cardiovascular diseases and cancer. Estrogens act with leptin, a satiety hormone encoded by the ob gene, to regulate energy homeostasis in females. Leptin-deficient mice (ob/ob) exhibit morbid obesity and insulin resistance. In addition to estrogens and leptin, the gut microbiome (gut microbes and their metabolites), is critical in regulating energy metabolism. The present study investigates whether estrogens and leptin modulate gut microbiota in ovariectomized ob/ob (obese) or heterozygote (lean) control mice fed a high-fat diet (HFD) that received either 17β-Estradiol (E2) or vehicle implants. E2 attenuated weight gain in both genotypes compared to vehicle counterparts. Moreover, both obesity (ob/ob mice) and E2 reduced gut microbial diversity. ob/ob mice exhibited lower species richness than control mice, while E2-treated mice had reduced evenness compared to vehicle mice. Regarding taxa, E2 treatment was associated with higher abundances of the family S24-7. Leptin was associated with higher abundances of Coriobacteriaceae, Clostridium and Lactobacillus. E2 and leptin had overlapping effects on relative abundances of some taxa, suggesting that interaction of these hormones is important in gut microbial homeostasis. Taken together, these findings suggest that E2 and leptin profoundly alter the gut microbiota of HFD-fed female mice. Understanding the function of E2 and leptin in regulating gut microbiota will allow the development of therapies targeting the gut microbiome for hormone-dependent metabolic disorders in women.

scholarly journals Specific knockout of p85α in brown adipose tissue induces resistance to high-fat diet–induced obesity and its metabolic complications in male mice

2020 ◽  
Vol 31 ◽  
pp. 1-13 ◽  
Author(s):  
Almudena Gomez-Hernandez ◽  
Andrea R. Lopez-Pastor ◽  
Carlota Rubio-Longas ◽  
Patrik Majewski ◽  
Nuria Beneit ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Male Mice ◽  
High Fat ◽  
Metabolic Complications ◽  
Diet Induced Obesity ◽  
Brown Adipose

scholarly journals Antiobesogenic Potential of Seaweed Dulse (Palmaria palmata) in High-fat Fed C57BL/6 J Mice (P21-014-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Rufa Mendez ◽  
Cristobal Miranda ◽  
Courtney Armour ◽  
Thomas Sharpton ◽  
Jan Frederik Stevens ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiome ◽  
Early Phase ◽  
Insulin Response ◽  
Palmaria Palmata ◽  
High Fat ◽  
Low Fat ◽  
Microbiome Analysis ◽  
Diet Induced Obesity ◽  
Lipid Excretion

Abstract Objectives The growing obesity challenge around the world continues to warrant interventions that could mitigate disease onset and progression. This study aimed to evaluate the potential of seaweed supplementation using dulse (Palmaria palmata) and wakame (Undaria pinnatifida), in improving caloric management and insulin resistance, and mitigating inflammation and gut microbiome shifts in diet-induced obesity in C57BL/6 J mice. Methods Twenty-four individually-caged C57BL/6 J mice were fed ad libitum with a high-fat diet (HFD) with and without seaweed inclusion, and another 8 mice for low-fat control (n = 8). Freeze-dried dulse and wakame were incorporated in the test diets at 5% inclusion level. Glucose tolerance test was performed during week 4 to assess insulin resistance state of test animals. After 9 weeks, fresh fecal samples were collected from all 32 mice prior to necropsy. These were used for the gut microbiome analysis using MiSeq. Fecal triglyceride levels were determined using Infinity Triglycerides Kit while plasma Monocyte Chemoattractant Protein-1 (MCP-1) was quantified using ELISA. Results Despite higher feed intake, dulse-fed mice had lower feed efficiency, indicating less weight gain from same amount of diet. This group also showed improved early-phase insulin response compared to HFD and wakame-fed groups. Plasma inflammatory marker MCP-1 levels were also significantly reduced in dulse-fed mice. While liver triglyceride levels were not affected with the dietary inclusion, fecal samples showed that there was higher lipid being excreted in dulse-fed group. This suggests that caloric excess and inflammatory progression may have been mitigated by increased lipid excretion in the feces. Gut microbiome analysis showed that dulse-fed mice retained microflora composition that is comparable to those fed with low-fat diet. Conclusions Our work reveals that dulse supplementation improved obesity and associated metabolic parameters by increasing lipid excretion, improving early-phase insulin response, and mitigating both inflammation and gut microbiome shifts associated with HFD, more effectively than wakame. These provide initial evidences that dietary inclusion of dulse holds therapeutic promise in mitigating diet-induced obesity. Funding Sources Oregon State University Agricultural Research Foundation. Supporting Tables, Images and/or Graphs

scholarly journals Effects and Mechanisms of Chitosan and ChitosanOligosaccharide on Hepatic Lipogenesis and Lipid Peroxidation, Adipose Lipolysis, and Intestinal Lipid Absorption in Rats with High-Fat Diet-Induced Obesity

2021 ◽  
Vol 22 (3) ◽  
pp. 1139
Author(s):  
Shing-Hwa Liu ◽  
Rui-Yi Chen ◽  
Meng-Tsan Chiang
Keyword(s):  
Lipid Peroxidation ◽  
High Fat Diet ◽  
Control Diet ◽  
Liver Lipid ◽  
Lipid Absorption ◽  
Chitosan Oligosaccharide ◽  
Hepatic Lipogenesis ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Liver Lipid Peroxidation

Chitosan and its derivative, chitosan oligosaccharide (CO), possess hypolipidemic and anti-obesity effects. However, it is still unclear if the mechanisms are different or similar between chitosan and CO. This study was designed to investigate and compare the effects of CO and high-molecular-weight chitosan (HC) on liver lipogenesis and lipid peroxidation, adipose lipolysis, and intestinal lipid absorption in high-fat (HF) diet-fed rats for 12 weeks. Rats were divided into four groups: normal control diet (NC), HF diet, HF diet+5% HC, and HF diet+5% CO. Both HC and CO supplementation could reduce liver lipid biosynthesis, but HC had a better effect than CO on improving liver lipid accumulation in HF diet-fed rats. The increased levels of triglyceride decreased lipolysis rate, and increased lipoprotein lipase activity in the perirenal adipose tissue of HF diet-fed rats could be significantly reversed by both HC and CO supplementation. HC, but not CO, supplementation promoted liver antioxidant enzymes glutathione peroxidase and superoxide dismutase activities and reduced liver lipid peroxidation. In the intestines, CO, but not HC, supplementation reduced lipid absorption by reducing the expression of fabp2 and fatp4 mRNA. These results suggest that HC and CO have different mechanisms for improving lipid metabolism in HF diet-fed rats.

scholarly journals Absence of muricholic acid due to Cyp2c-deficiency protects against high fat diet-induced obesity in male mice but promotes liver damage

2021 ◽  
Author(s):  
Antwi-Boasiako Oteng ◽  
Sei Higuchi ◽  
Alexander S. Banks ◽  
Rebecca A. Haeusler
Keyword(s):  
Liver Damage ◽  
High Fat Diet ◽  
Energy Content ◽  
Lipid Absorption ◽  
Chow Diet ◽  
Male Mice ◽  
Wild Type ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Obesogenic Diet

Objective: Murine-specific muricholic acids (MCAs) are reported to protect against obesity and associated metabolic disorders. However, the response of mice with genetic depletion of MCA to an obesogenic diet has not been evaluated. We used Cyp2c-deficient (Cyp2c-/-) mice, which lack MCAs and thus have a human-like bile acid (BA) profile, to directly investigate the potential role of MCAs in diet-induced obesity. Methods: Male and female Cyp2c-/- mice and wild-type controls were fed a standard chow diet or a high fat diet (HFD) for 18 weeks. We measured BA composition from a pool of liver, gallbladder, and intestine, as well as weekly body weight, food intake, lean and fat mass, systemic glucose homeostasis, energy expenditure, intestinal lipid absorption, fecal lipid, and energy content. Results: Cyp2c deficiency depleted MCAs and caused other changes in BA composition, namely a decrease in the ratio of 12α-hydroxylated (12α-OH) BAs to non-12α-OH BAs, without altering the total BA levels. While wild-type male mice became obese after HFD-feeding, Cyp2c-/- male mice were protected from obesity and associated metabolic dysfunctions. Cyp2c-/- male mice also showed reduced intestinal lipid absorption and increased lipid excretion, which was reversed by oral gavage with the 12α-OH BA, taurocholic acid. Cyp2c-/- mice also showed increased liver damage, which appeared stronger in females. Conclusion: MCA does not protect against diet-induced obesity but may protect against liver injury. Reduced lipid absorption in Cyp2c-deficient male mice is potentially due to a reduced ratio of 12α-OH/non-12α-OH BAs.

Protection against diet-induced obesity and obesity- related insulin resistance in Group 1B PLA2-deficient mice

2002 ◽  
Vol 283 (5) ◽  
pp. E994-E1001 ◽  
Author(s):  
Kevin W. Huggins ◽  
Amy C. Boileau ◽  
David Y. Hui
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Dietary Lipids ◽  
Lipid Absorption ◽  
Lipolytic Enzyme ◽  
Fat Absorption ◽  
High Fat ◽  
Lower Plasma ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

Group 1B phospholipase A2 (PLA2) is an abundant lipolytic enzyme that is well characterized biochemically and structurally. Because of its high level of expression in the pancreas, it has been presumed that PLA2 plays a role in the digestion of dietary lipids, but in vivo data have been lacking to support this theory. Our initial study on mice lacking PLA2demonstrated no abnormalities in dietary lipid absorption in mice consuming a chow diet. However, the effects of PLA2deficiency on animals consuming a high-fat diet have not been studied. To investigate this, PLA2 +/+ and PLA2 −/− mice were fed a western diet for 16 wk. The results showed that PLA2 −/− mice were resistant to high-fat diet-induced obesity. This observed weight difference was due to decreased adiposity present in the PLA2 −/− mice. Compared with PLA2 +/+ mice, the PLA2 −/− mice had 60% lower plasma insulin and 72% lower plasma leptin levels after high-fat diet feeding. The PLA2 −/− mice also did not exhibit impaired glucose tolerance associated with the development of obesity-related insulin resistance as observed in the PLA2 +/+ mice. To investigate the mechanism by which PLA2 −/− mice exhibit decreased weight gain while on a high-fat diet, fat absorption studies were performed. The PLA2 −/− mice displayed 50 and 35% decreased plasma [3H]triglyceride concentrations 4 and 6 h, respectively, after feeding on a lipid-rich meal containing [3H]triolein. The PLA2 −/− mice also displayed increased lipid content in the stool, thus indicating decreased fat absorption in these animals. These results suggest a novel role for PLA2 in the protection against diet-induced obesity and obesity-related insulin resistance, thereby offering a new target for treatment of obesity and diabetes.

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