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In this study, lactic acid bacterium, Lactobacillus plantarum KFY04, was isolated from Xinjiang yogurt, and it was used to intervene in obese mice maintained on a 45% fat diet, and we compared its effects to those of a commercial strain, LDSB, and l-carnitine. The results showed that the LP-KFY04 intervention mice gained weight more slowly and had lower liver, epididymal adipose, and perirenal adipose tissue indices when compared to the other high-fat groups. Moreover, the LP-KFY04 can reduce the formation of fat vacuoles in the liver, while also reducing adipocyte differentiation and volume, and LP-KFY04 groups had the lowest liver and serum AST, ALT, TG, and TC levels and lowest serum LDL-C and highest HDL-C levels among the groups maintained on a high-fat diet. LP-KFY04 was also shown to mitigate obesity-associated oxidative damage and inflammatory responses. Additionally, quantitative real-time PCR and western blot analysis examining liver and adipose tissue expression of PPAR-α, CYP7A1, CPT1, and LPL showed an increased expression in the LP-KFY04 groups while decreased expression levels of PPAR-γ and C/EBPα relative to the other high-fat diet groups. These results show that of the different interventions, LP-KFY04 was the most effective at mitigating the effects of obesity than LDSB and l-carnitine. The results confirmed that LP-KEY04 has better anti-obesity, anti-oxidative, and anti-inflammatory effects than current fermentation strains. It indicates LP-KFY04 is a fermentation strain with potential practical value and high functionality, and it shows that a fermentation strain should not only have good fermentation performance, but, more importantly, it must provide more functionality on the basis of fermentation.

Diet and host genetics influence the composition of intestinal microbiota, yet few studies have compared the function of intestinal microbiota in the diet- or genotype-induced lipid deposition, which limits our understanding of the role of intestinal bacteria in metabolic disorders. The lipid accumulation in wild-type zebrafish fed with control (CON) or high-fat (HF) diet and two gene-knockout zebrafish lines (cpt1b –/– or pparab –/–) fed with control diet was measured after a 4-week feeding experiment. The intestinal microbiota composition of these groups was investigated using 16S ribosomal RNA (rRNA) gene sequencing (DNA-based) and 16S rRNA sequencing (RNA-based). The HF diet or deficiency of two genes induced more weight gain and higher triglyceride content in the liver compared with their control group. 16S rRNA gene sequencing (DNA-based) indicated the decreased abundance of Proteobacteria in the HF group compared with CON, but there was no significant difference in bacterial α diversity among treatments. 16S rRNA sequencing (RNA-based) confirmed the decreased abundance of Proteobacteria and the bacterial α diversity in the HF group compared with CON. Deficiency of cpt1b or pparab showed less change in microbiota composition compared with their wild-type group. Intestinal microbiota of each group was transferred to germ-free zebrafish, and the quantification of Nile red staining indicated that the intestinal microbiota of the HF group induced more lipid accumulation compared with CON, whereas intestinal microbiota of cpt1b –/– and pparab –/– zebrafish did not. The results showed that RNA-based bacterial sequencing revealed more bacterial alteration than DNA-based bacterial sequencing. HF diet had a more dominant role in shaping gut microbiota composition to induce lipid accumulation compared with the gene-knockout of cpt1b or pparab in zebrafish, and the transplant of intestinal microbiota from HF-fed fish induced more lipid deposition in germ-free zebrafish. Together, these data suggested that a high-fat diet exerted a more dominant role over the deletion of cpt1b or pparab on the intestinal bacterial composition, which corresponded to lipid accumulation. [ABSTRACT FROM AUTHOR]

Background: Obesity is an epidemic disease in the world, the treatment and prevention of obesity methods have gained great attention. Lactobacillus is the main member of probiotics, and the physiological activity of it is specific to different strains. This study systematically explored the anti-obesity effect and possible mechanism of Lactobacillus fermentum CQPC07 (LF-CQPC07), which was isolated from pickled vegetables. Results: LF-CQPC07 effectively controlled the weight gain of mice caused by a high-fat diet. The results of pathological sections indicated that LF-CQPC07 alleviated hepatocyte damage and fat accumulation in adipocytes. The detection of biochemical indictors revealed that LF-CQPC07 decreased the levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG), and increased the level of high-density lipoprotein cholesterol (HDL-C). Additionally, LF-CQPC07 caused the decrease in the amounts of inflammatory cytokines interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, and interferon-γ (IFN-γ), and the increase in the amounts of the anti-inflammatory cytokines IL-10 and IL-4. LF-CQPC07 also decreased the amounts of alanine aminotransferase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP). Confirmed by qPCR, LF-CQPC07 enhanced the mRNA expression of catalase (CAT), gamma glutamylcysteine synthetase 1 (GSH1), copper/zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), and glutathione peroxidase (GSH-Px). It also increased the mRNA expression levels of carnitine palmitoyltransferase 1 (CPT1), peroxisome proliferator-activated receptor alpha (PPAR-α), lipoprotein lipase (LPL), and cholesterol 7 alpha hydroxylase (CYP7A1), and decreased that of PPAR-γ and CCAAT/enhancer binding protein alpha (C/EBP-α) in the liver of mice. Conclusion: This research confirmed that LF-CQPC07 is capable of ameliorating obesity, improving hyperlipemia, and alleviating chronic low-grade inflammation and liver injury accompanied with obesity. Its mechanism may be the regulation of antioxidant capacity and lipid metabolism. Therefore, LF-CQPC07 has enormous potential to serve as a potential probiotic for the prevention or treatment of obesity. [ABSTRACT FROM AUTHOR]

Lactic acid bacteria (LAB) are an important group of microorganisms in the food industry. LAB with health benefits are considered natural elements promoting consumer health. The study investigated the anti‐obesity effects of Lactobacillus plantarum CQPC01 (LP‐CQPC01) on high‐fat diet‐induced mice. Liver morphology, liver function indexes, lipid indexes, and inflammatory factors in the serum and liver were determined. Expressions of lipid metabolism‐related gene were also detected by qPCR. LP‐CQPC01 slowed the HFD‐induced increase in body weight, decreased the organ indexes, alleviated hepatic lipid accumulation, and inhibited the increased adipose cell volume. LP‐CQPC01 decreased lipid levels of serum and liver, and the contents of pro‐inflammatory factors, and increased the IL‐4 and IL‐10 contents. LP‐CQPC01 downregulated the expressions of the C/EBP‐α and PPARγ mRNA and upregulated CYP7A1, CPT1, LPL, CAT, SOD1, and SOD2 mRNA. Our results indicated that LP‐CQPC01 is a potential probiotic for preventing or alleviating high‐energy intake‐related lipid conditions. Practical applications: Obesity is a factor of a variety of cardiovascular diseases. Therefore, it is necessary to suppress the occurrence of fat accumulation in time. This study investigated the effect of LP‐CQPC01 on lipid regulation in mice fed a high‐fat diet (HFD) and clarified the mechanism of strain to alleviate obesity by enhancing the decomposition of cholesterol and detoxification of fat. LP‐CQPC01 reduced fat accumulation without oxidative damage, and was confirmed by the attenuated pathological changes of liver. This research can serve as a significant reference for future research, prevention, and treatment of high‐energy intake‐related lipid conditions, and the development of functional foods with anti‐obesity activity. [ABSTRACT FROM AUTHOR]

Probiotics are regard as safety approaches for preventing and treating some chronic diseases. This study investigated the regulating effect of Lactobacillus plantarum CQPC03 (LP‐CQPC03) on lipid metabolism in high‐fat diet (HFD)‐induced obesity in mice. The results showed that administration of LP‐CQPC03 at a concentration of 1.0 × 109 CFU/kg body weight inhibits HFD‐induced obesity and improves lipid metabolism in the liver and serum. LP‐CQPC03 intervention attenuated obesity‐induced hepatic tissue damage, led decreases in hepatic triglyceride (42.02 mmol/gprot), total cholesterol (3.85 mmol/gprot), and LDL‐C (1.03 mmol/gprot), and an increase in HDL‐C (1.07 mmol/gprot). The same tendencies were observed in serum of HFD‐fed mice. LP‐CQPC03 intervention led a decrease in serum levels of aspartic transaminase, alanine transaminase, and alkaline phosphatase. LP‐CQPC03 alleviated inflammation by increasing the level of interleukin (IL)‐4 and IL‐10, and decreasing the levels of pro‐inflammatory factors, including IL‐6, IL‐1β, tumor necrosis factor‐α, and interferon‐γ. LP‐CQPC03 also increased activities of SOD and GSH‐Px in liver significantly and dropped the hepatic malondialdehyde (MDA) level from 3.39 nmol/gprot to 1.90 nmol/gprot. RT‐qPCR results showed that the lipid metabolism‐improving effect of LP‐CQPC03 was performed by upregulating the expression of carnitine palmitoyltransferase 1, lipoprotein lipase, catalase, and superoxide dismutase 1. This study indicates that L. plantarum CQPC03 might be a potential probiotic that can help mitigate the adverse effects of excessive lipids on the liver, and prevent or alleviate high‐energy intake‐related obesity. Practical applications: Intaking high‐energy foods is a potential risk of lipid metabolic disorder. Therefore, it is necessary to seek an effective and safe approach for preventing the obesity‐related disease. This study found that LP‐CQPC03 limited the rate of increase in body weight of mice fed on HFD, maintained normal hepatic tissue morphology, and exhibited a strong regulating effect on lipid metabolism. And the threshold concentration of LP‐CQPC03 for the lipid‐lowering effect was 1.0 × 109 CFU/kg body weight. Therefore, LP‐CQPC03 is a potential probiotic for preventing or alleviating high‐energy intake‐related obesity. [ABSTRACT FROM AUTHOR]

Malus hupehensis leaves (MHL) are used to make traditional Chinese tea. In this study, MHL extract was shown to improve metabolic disorders and inflammatory response in high‐fat diet‐induced obese mice. MHL extract could reduce body weight, and significantly alleviate liver damage and fat accumulation. MHL extract caused a decrease in the levels of ALT, AST, AKP, TC, TG, LDL‐C, and an increase in the level of HDL‐C. It also caused a decrease in inflammatory cytokines, including TNF‐α, IFN‐γ, IL‐1β, IL‐6, and an increase in the anti‐inflammatory cytokine IL‐10 and IL‐4. MHL extract could upregulate mRNA expression of PPAR‐α, LPL, CPT1, CYP7A1, SOD1, SOD2, CAT, GSH1, and GSH‐Px and downregulate that of PPAR‐γ and C/EBP‐α in the liver of obese mice. In conclusion, our work represents the first study demonstrating that MHL extract possesses an anti‐obesity effect and alleviates obesity‐related symptoms, including dyslipidemia, chronic low‐grade inflammatory, and liver damage. Practical applications: The research may contribute to the development and application of MHL as functional foods or dietary supplement to fight against obesity. [ABSTRACT FROM AUTHOR]

Small‐leaved Kuding tea (SLKDT; Ligustrum robustum) is a traditional Chinese tea. We systematically investigated the effect of SLKDT extract on obesity. SLKDT‐controlled weight gain in mice fed a high‐fat diet. Tissue specimen results showed that the SLKDT extract alleviated liver damage and fat accumulation. Meanwhile, SLKDT extract improved dyslipidemia by decreasing total cholesterol, triglycerides, and low‐density lipoprotein cholesterol levels and increasing high‐density lipoprotein cholesterol levels. Furthermore, SLKDT extract reduced alanine aminotransferase, alkaline phosphatase, and aspartate transaminase levels in the serum and liver tissues; decreased inflammatory cytokines, including interleukin (IL)‐1β, tumor necrosis factor‐α, interferon‐γ, and IL‐6; and increased the anti‐inflammatory cytokines, IL‐4 and IL‐10. The quantitative PCR results showed that SLKDT extract upregulated the mRNA expressions of peroxisome proliferator‐activated receptor (PPAR)‐α, lipoprotein lipase, carnitine palmitoyltransferase 1, and cholesterol 7 alpha hydroxylase and downregulated PPAR‐γ and CCAAT/enhancer‐binding protein‐alpha mRNA expressions in the obese mouse livers to reduce adipocyte differentiation and fat accumulation, promote fat oxidation, and improve dyslipidemia, thereby inhibiting the immune response and alleviating liver injury. SLKDT shows a potential for preventing obesity and regulating obesity‐related syndrome, so it is possible to be further developed as a novel treatment for fighting obesity. [ABSTRACT FROM AUTHOR]