Adiponectin administration prevents weight gain and glycemic profile changes in diet-induced obese immune deficient Rag1−/− mice lacking mature lymphocytes

Liu, Xiaowen; Perakakis, Nikolaos; Gong, Hui; Chamberland, John P.; Brinkoetter, Mary; Hamnvik, Ole-Petter R; Mantzoros, Christos S.

doi:10.1016/j.metabol.2016.09.003

Cited by 16 publications

(11 citation statements)

References 40 publications

(55 reference statements)

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“…Mice in DSS and DA groups received 4% DSS (average molecular weight 5000, Sigma-Aldrich) instead for tap water to establish IBD model [15]. Mice in AG and DA groups were intraperitoneally administrated with full-length adiponectin (2 µg/g, 0.2 ml/mouse) [16]. The control and untreated challenged animals received the same volume of saline alone.…”

Section: Methodsmentioning

confidence: 99%

RETRACTED ARTICLE: Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

Zhao

Liu²,

Tan

et al. 2018

Inflamm. Res.

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BackgroundAdiponectin, a protein hormone produced by adipose tissues, exhibits anti-inflammatory functions in various models. This study was investigated the effects of adiponectin on dextran sodium sulfate (DSS)-colonic injury, inflammation, apoptosis, and intestinal barrier dysfunction in Caco-2 cell and mice.Materials and methodsThe results showed that DSS caused inflammatory response and intestinal barrier dysfunction in vitro and in vivo. Adiponectin injection alleviated colonic injury and rectal bleeding in mice. Meanwhile, adiponectin downregulated colonic IL-1β and TNF-α expressions and regulated apoptosis relative genes to attenuate DSS-induced colonic inflammation and apoptosis. Adiponectin markedly reduced serum lipopolysaccharide concentration, a biomarker for intestinal integrity, and enhanced colonic expression of tight junctions (ZO-1 and occludin). The in vitro data further demonstrated that adiponectin alleviated DSS-induced proinflammatory cytokines production and the increased permeability in Caco-2 cells.ConclusionAdiponectin plays a beneficial role in DSS-induced inflammation via alleviating apoptosis and improving intestinal barrier integrity.

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Section: Methodsmentioning

confidence: 99%

RETRACTED ARTICLE: Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

Zhao

Liu²,

Tan

et al. 2018

Inflamm. Res.

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“…(29,30) Adiponectin stimulates fatty acid oxidation, decreases inflammation and fibrosis, and improves insulin sensitivity. (31)(32)(33) Adiponectin levels progressively decrease from NAFL to NASH and have been used to develop noninvasive diagnostic tools for staging NAFLD. (34,35) Treatment with CHS-131 increased the circulating levels of adiponectin ~2.4fold, which is similar to the increase observed in humans treated with pioglitazone.…”

Section: Discussionmentioning

confidence: 99%

The Selective Peroxisome Proliferator‐Activated Receptor Gamma Modulator CHS‐131 Improves Liver Histopathology and Metabolism in a Mouse Model of Obesity and Nonalcoholic Steatohepatitis

et al. 2020

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CHS‐131 is a selective peroxisome proliferator‐activated receptor gamma modulator with antidiabetic effects and less fluid retention and weight gain compared to thiazolidinediones in phase II clinical trials. We investigated the effects of CHS‐131 on metabolic parameters and liver histopathology in a diet‐induced obese (DIO) and biopsy‐confirmed mouse model of nonalcoholic steatohepatitis (NASH). Male C57BL/6JRj mice were fed the amylin liver NASH diet (40% fat with trans‐fat, 20% fructose, and 2% cholesterol). After 36 weeks, only animals with biopsy‐confirmed steatosis and fibrosis were included and stratified into treatment groups (n = 12‐13) to receive for the next 12 weeks (1) low‐dose CHS‐131 (10 mg/kg), (2) high‐dose CHS‐131 (30 mg/kg), or (3) vehicle. Metabolic parameters, liver pathology, metabolomics/lipidomics, markers of liver function and liver, and subcutaneous and visceral adipose tissue gene expression profiles were assessed. CHS‐131 did not affect body weight, fat mass, lean mass, water mass, or food intake in DIO‐NASH mice with fibrosis. CHS‐131 improved fasting insulin levels and insulin sensitivity as assessed by the intraperitoneal insulin tolerance test. CHS‐131 improved total plasma cholesterol, triglycerides, alanine aminotransferase, and aspartate aminotransferase and increased plasma adiponectin levels. CHS‐131 (high dose) improved liver histology and markers of hepatic fibrosis. DIO‐NASH mice treated with CHS‐131 demonstrated a hepatic shift to diacylglycerols and triacylglycerols with a lower number of carbons, increased expression of genes stimulating fatty acid oxidation and browning, and decreased expression of genes promoting fatty acid synthesis, triglyceride synthesis, and inflammation in adipose tissue. Conclusion: CHS‐131 improves liver histology in a DIO and biopsy‐confirmed mouse model of NASH by altering the hepatic lipidome, reducing insulin resistance, and improving lipid metabolism and inflammation in adipose tissue.

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“…It is noteworthy that transgenic mice, which were morbidly obese (MO), had increased levels of circulating full-length adiponectin and showed a constriction in systemic inflammation and an improved metabolic profile [ 26 ]. Treatment with adiponectin reduces body weight and blood glucose levels in obese mice fed a high fat diet [ 27 28 ]. This is achieved by improving insulin sensitivity [ 27 ], increasing fat oxidation and regulating inflammatory response mainly through innate rather than adaptive immune system mechanisms [ 28 ].…”

Section: Adiponectinmentioning

confidence: 99%

Association of Adipokines with Development and Progression of Nonalcoholic Fatty Liver Disease

2018

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Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease affecting 30% of the general population and 40% to 70% of obese individuals. Adipose tissue plays a crucial role in its pathogenesis, as it produces and secretes pro- and anti-inflammatory cytokines called adipokines. Adiponectin and leptin have well-determined actions in terms of NAFLD pathophysiology. Adiponectin deficiency is associated with a pro-inflammatory condition, as it is observed in obesity and other metabolic disorders. On the other hand, increased leptin levels, above the normal levels, act as a pro-inflammatory stimulus. Regarding other adipokines (resistin, visfatin, chemerin, retinol-binding protein 4, irisin), data about their contribution to NAFLD pathogenesis and progression are inconclusive. In addition, pharmacological agents like thiazolidinediones (pioglitazone and rosiglitazone), that are used in the management of NAFLD exert favourable effects on adipokine levels, which in turn may contribute to the improvement of liver function. This review summarizes the current knowledge and developments in the association between adipokines and NAFLD and discusses possible therapeutic implications targeting the modulation of adipokine levels as a potential tool for the treatment of NAFLD.

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Adiponectin administration prevents weight gain and glycemic profile changes in diet-induced obese immune deficient Rag1−/− mice lacking mature lymphocytes

Cited by 16 publications

References 40 publications

RETRACTED ARTICLE: Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

RETRACTED ARTICLE: Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

The Selective Peroxisome Proliferator‐Activated Receptor Gamma Modulator CHS‐131 Improves Liver Histopathology and Metabolism in a Mouse Model of Obesity and Nonalcoholic Steatohepatitis

Association of Adipokines with Development and Progression of Nonalcoholic Fatty Liver Disease

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