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Probiotics improve high fat diet-induced hepatic steatosis and insulin resistance by increasing hepatic NKT cells.

ABSTRACT: Dietary factors and intestinal bacteria play an important role in the rapidly increasing incidence of obesity and its associated conditions, such as steatosis and insulin resistance. In the current study, we evaluated the effect of probiotics, and their mechanisms on diet-induced obesity, steatosis and insulin resistance.Wild-type male C57BL6 mice were fed either normal or high fat diets. Some mice received VSL#3 probiotics. Animal weight, hepatic steatosis, insulin resistance, and their relationship to hepatic Natural Killer T cells (NKT) cell number and inflammatory signaling were evaluated.High fat diet induced a depletion of hepatic NKT cells thus leading to insulin resistance and steatosis. Oral probiotic treatment significantly improved the high fat diet-induced hepatic NKT cell depletion, insulin resistance and hepatic steatosis. This effect was NKT cell dependant, resulted from the attenuation of the tumor necrosis factor-alpha and IkappaB kinase inflammatory signaling, and led to an improved sensitivity in insulin signaling.Probiotics improve high fat diet-induced steatosis and insulin resistance. These effects of probiotics are likely due to increased hepatic NKT cell numbers and reduced inflammatory signaling.

SUBMITTER: Ma X

PROVIDER: S-EPMC2588670 | biostudies-literature | 2008 Nov

REPOSITORIES: biostudies-literature

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Probiotics improve high fat diet-induced hepatic steatosis and insulin resistance by increasing hepatic NKT cells.

Ma Xiong X Hua Jing J Li Zhiping Z

Journal of hepatology 20080630 5

<h4>Background/aims</h4>Dietary factors and intestinal bacteria play an important role in the rapidly increasing incidence of obesity and its associated conditions, such as steatosis and insulin resistance. In the current study, we evaluated the effect of probiotics, and their mechanisms on diet-induced obesity, steatosis and insulin resistance.<h4>Methods</h4>Wild-type male C57BL6 mice were fed either normal or high fat diets. Some mice received VSL#3 probiotics. Animal weight, hepatic steatosi ...[more]

PMID: 18674841

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Project description:Background/objectivesVisceral adiposity is associated with increased diabetes risk, while expansion of subcutaneous adipose tissue may be protective. However, the visceral compartment contains different fat depots. Peripancreatic adipose tissue (PAT) is an understudied visceral fat depot. Here, we aimed to define PAT functionality in lean and high-fat-diet (HFD)-induced obese mice.Subjects/methodsFour adipose tissue depots (inguinal, mesenteric, gonadal, and peripancreatic adipose tissue) from chow- and HFD-fed male mice were compared with respect to adipocyte size (n = 4-5/group), cellular composition (FACS analysis, n = 5-6/group), lipogenesis and lipolysis (n = 3/group), and gene expression (n = 6-10/group). Radioactive tracers were used to compare lipid and glucose metabolism between these four fat depots in vivo (n = 5-11/group). To determine the role of PAT in obesity-associated metabolic disturbances, PAT was surgically removed prior to challenging the mice with HFD. PAT-ectomized mice were compared to sham controls with respect to glucose tolerance, basal and glucose-stimulated insulin levels, hepatic and pancreatic steatosis, and gene expression (n = 8-10/group).ResultsWe found that PAT is a tiny fat depot (~0.2% of the total fat mass) containing relatively small adipocytes and many "non-adipocytes" such as leukocytes and fibroblasts. PAT was distinguished from the other fat depots by increased glucose uptake and increased fatty acid oxidation in both lean and obese mice. Moreover, PAT was the only fat depot where the tissue weight correlated positively with liver weight in obese mice (R = 0.65; p = 0.009). Surgical removal of PAT followed by 16-week HFD feeding was associated with aggravated hepatic steatosis (p = 0.008) and higher basal (p < 0.05) and glucose-stimulated insulin levels (p < 0.01). PAT removal also led to enlarged pancreatic islets and increased pancreatic expression of markers of glucose-stimulated insulin secretion and islet development (p < 0.05).ConclusionsPAT is a small metabolically highly active fat depot that plays a previously unrecognized role in the pathogenesis of hepatic steatosis and insulin resistance in advanced obesity.

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Probiotics improve high fat diet-induced hepatic steatosis and insulin resistance by increasing hepatic NKT cells.

Publications

Probiotics improve high fat diet-induced hepatic steatosis and insulin resistance by increasing hepatic NKT cells.

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