scholarly journals Lactobacillus Brevis OPK-3 from Kimchi Prevents Obesity and Modulates the Expression of Adipogenic and Pro-Inflammatory Genes in Adipose Tissue of Diet-Induced Obese Mice

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 604 ◽  
Author(s):  
Jung Eun Park ◽  
Suk-Heung Oh ◽  
Youn-Soo Cha

Our previous study reported that lactic acid bacteria (L. brevis OPK-3) isolated from kimchi ameliorated intracellular lipid accumulation in 3T3-L1 adipocyte. The current study explored potential roles of L. brevis OPK-3 (KLAB) on preventing body weight gain and its effect on the inflammatory response of adipose tissue. Male C57BL/6 mice (n = 10) were divided into four groups: normal diet with distilled water (NDC), high-fat diet with distilled water (HDC), high-fat diet with L-ornithine (OTC) or high-fat diet with KLAB. The KLAB supplement resulted in significantly lower body weight, lower epididymal fat tissue mass, and lower serum and hepatic TG levels than the HDC. KLAB supplementation improved serum cytokines, and real-time polymerase chain reaction (PCR) analysis showed significantly lower inflammatory cytokine mRNA levels in epididymal adipose tissue. These results suggest that the administration of KLAB inhibits the induction of inflammation in adipose tissue along with the inhibition of weight gain. Therefore, this study demonstrates the therapeutic and beneficial value of this strain produced during the fermentation of kimchi.

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Ying Shen ◽  
Su Jin Song ◽  
Narae Keum ◽  
Taesun Park

The present study aimed to investigate whether olive leaf extract (OLE) prevents high-fat diet (HFD)-induced obesity in mice and to explore the underlying mechanisms. Mice were randomly divided into groups that received a chow diet (CD), HFD, or 0.15% OLE-supplemented diet (OLD) for 8 weeks. OLD-fed mice showed significantly reduced body weight gain, visceral fat-pad weights, and plasma lipid levels as compared with HFD-fed mice. OLE significantly reversed the HFD-induced upregulation of WNT10b- and galanin-mediated signaling molecules and key adipogenic genes (PPARγ, C/EBPα, CD36, FAS, and leptin) in the epididymal adipose tissue of HFD-fed mice. Furthermore, the HFD-induced downregulation of thermogenic genes involved in uncoupled respiration (SIRT1, PGC1α, and UCP1) and mitochondrial biogenesis (TFAM, NRF-1, and COX2) was also significantly reversed by OLE. These results suggest that OLE exerts beneficial effects against obesity by regulating the expression of genes involved in adipogenesis and thermogenesis in the visceral adipose tissue of HFD-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

2007 ◽  
Vol 97 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Patricia Pérez-Matute ◽  
Nerea Pérez-Echarri ◽  
J. Alfredo Martínez ◽  
Amelia Marti ◽  
María J. Moreno-Aliaga

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.


2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Meilin Hu ◽  
Fan Wu ◽  
Jinlong Luo ◽  
Jing Gong ◽  
Ke Fang ◽  
...  

Berberine (BBR) is the main active ingredient of a traditional Chinese herb Coptis chinensis. It has been reported to exhibit beneficial effects in treating diabetes and obesity. However, the underlying mechanism has not been fully elucidated. Adipose tissue fibrosis is a hallmark of obesity-associated adipose tissue dysfunction. HIF-1α plays a key role in adipose tissue fibrosis, which closely linked to metabolic dysfunction in obese state. We hypothesized that BBR may alleviate obesity-induced adipose tissue fibrosis and associated metabolic dysfunction through inhibition of HIF-1α. To test this hypothesis, we treated high fat diet (HFD) feeding mice with different dose of BBR (100 mg/kg, 200 mg/kg, and 300 mg/kg) for 8 weeks. We found that BBR treatment greatly decreased the body weight gain and reduced insulin resistance induced by HFD. Data also revealed that BBR improved histologic fibrous of epididymal white adipose tissue (eWAT) and was accompanied with inhibition of the abnormal synthesis and deposition of extracellular matrix (ECM) proteins, such as collagen and fibronectin. We also found that BBR treatment suppressed the expression of HIF-1α and decreased the mRNA expression of LOX in epididymal adipose tissue, which plays a key role in fibrosis development. Taken together, these results suggest that BBR can regulate metabolic homeostasis and suppress adipose tissue fibrosis through inhibiting the expression of HIF-1α.


1999 ◽  
Vol 58 (4) ◽  
pp. 773-777 ◽  
Author(s):  
John E. Blundell ◽  
John Cooling

It is now widely accepted that obesity develops by way of genetic mechanisms conferring specific dispositions which interact with strong environmental pressures. It is also accepted that certain dispositions constitute metabolic risk factors for weight gain. It is less well accepted that certain patterns of behaviour (arising from biological demands or environmental influences) put individuals at risk of developing a positive energy balance and weight gain (behavioural risk factors). Relevant patterns of behaviour include long-lasting habits for selecting and eating particular types of foods. Such habits define two distinct groups characterized as high-fat (HF) and low-fat (LF) phenotypes. These habits are important because of the attention given to dietary macronutrients in body-weight gain and the worldwide epidemic of obesity. Considerable evidence indicates that the total amount of dietary fat consumed remains the most potent food-related risk factor for weight gain. However, although habitual intake of a high-fat diet is a behavioural risk factor for obesity, it does not constitute a biological inevitability. A habitual low-fat diet does seem to protect against the development of obesity, but a high-fat diet does not guarantee that an individual will be obese. Although obesity is much more prevalent among HF than LF, some HF are lean with BMI well within the normal range. The concept of 'different routes to obesity' through a variety of nutritional scenarios can be envisaged, with predisposed individuals varying in their susceptibility to different dietary inputs. In a particular subgroup of individuals (young adult males) HF and LF displayed quite different profiles of appetite control, response to nutrient challenges and physiological measures, including BMR, RQ, heart rate, plasma leptin levels and thermogenic responses to fat and carbohydrate meals. These striking differences suggest that HF and LF can be used as a conceptual tool to investigate the relationship between biology and the environment (diet) in the control of body weight.


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