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Impact of A Cargo-Less Liposomal Formulation on Dietary Obesity-Related Metabolic Disorders in Mice.

ABSTRACT: Current therapeutic options for obesity often require pharmacological intervention with dietary restrictions. Obesity is associated with underlying inflammation due to increased tissue macrophage infiltration, and recent evidence shows that inflammation can drive obesity, creating a feed forward mechanism. Therefore, targeting obesity-induced macrophage infiltration may be an effective way of treating obesity. Here, we developed cargo-less liposomes (UTS-001) using 1,2-dioleoyl-sn-glycero-3-phosphocholine, DOPC (synthetic phosphatidylcholine) as a single-agent to manage weight gain and related glucose disorders due to high fat diet (HFD) consumption in mice. UTS-001 displayed potent immunomodulatory properties, including reducing resident macrophage number in both fat and liver, downregulating liver markers involved in gluconeogenesis, and increasing marker involved in thermogenesis. As a result, UTS-001 significantly enhanced systemic glucose tolerance in vivo and insulin-stimulated cellular glucose uptake in vitro, as well as reducing fat accumulation upon ad libitum HFD consumption in mice. UTS-001 targets tissue residence macrophages to suppress tissue inflammation during HFD-induced obesity, resulting in improved weight control and glucose metabolism. Thus, UTS-001 represents a promising therapeutic strategy for body weight management and glycaemic control.

SUBMITTER: Komalla V

PROVIDER: S-EPMC7589567 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Impact of A Cargo-Less Liposomal Formulation on Dietary Obesity-Related Metabolic Disorders in Mice.

Komalla Varsha V Sheikholeslami Behjat B Li Gerard G Bokshi Bishwajit B Chan Yik Lung YL Ung Alison A Gregory Oliver Brian B Chen Hui H Haghi Mehra M

International journal of molecular sciences 20201015 20

Current therapeutic options for obesity often require pharmacological intervention with dietary restrictions. Obesity is associated with underlying inflammation due to increased tissue macrophage infiltration, and recent evidence shows that inflammation can drive obesity, creating a feed forward mechanism. Therefore, targeting obesity-induced macrophage infiltration may be an effective way of treating obesity. Here, we developed cargo-less liposomes (UTS-001) using 1,2-dioleoyl-sn-glycero-3-phos ...[more]

PMID: 33076522

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Project description:Thiamine prevents diabetic complications, and its deficiency, resulting from mutation of thiamine transporter gene SLC19A2 has been linked to diabetes mellitus. We previously found that thiamine mitigates metabolic disorders in spontaneous hypertensive rats, harboring defects in glucose and fatty acid metabolism. The current study extends our hypothesis that that thiamine intervention may impact metabolic abnormalities in polyphagia-induced Otsuka Long-Evans Tokushima Fatty (OLETF) rats that lack functional cholecystokinin A receptors. Male OLETF rats exhibit progressive obesity and metabolic disorders similar to human metabolic syndrome. Male OLETF rats (4-week-old) were given free access to water containing either 0.2 % or 0 % of thiamine for 51 weeks. At the end of treatment, blood parameters and cardiac functions were analyzed. After sacrifice, the organs were removed and weights of organs and histological findings were evaluated. In addition, differential gene expression in the liver was analyzed. Thiamine intervention averted obesity, mainly resulting from reduction of visceral adiposity, and prevented metabolic disorders in OLETF rats. Histological evaluation revealed that thiamine alleviated adipocyte hypertrophy, steatosis in the liver, heart, and skeletal muscle, interstitial fibrosis in the heart and kidney, fatty degeneration in the pancreas, thickening of the basement membrane of vasculature, and glomerulopathy and mononuclear cell infiltration in the kidney. Cardiac and renal functions were preserved in thiamine treatment. Seventy-six genes showed at least two-fold difference in hepatic expression with thiamine treatment. Several of them participated in carbohydrate metabolism (Hk1, Pygb, Slc2a8, Rtn4, Rhbdl1, and Tspan8), lipid metabolism (Pla2g15, Por, and Lmf1), vascular physiology (S1pr1, Epha8, Rtn4, Slc7a13, Cdh15, Itga9, Cd151, Cd40lg, Nid1 and Lamb1), and carcinogenesis (Lmo7, Fgfr3, and Dmbt1). Modification of transcript expression well accorded with the findings of blood parameters and organ morphologies. Thiamine prevented polyphagia-induced obesity and metabolic and functional disorders in OLETF rats.

Dataset Information

Impact of A Cargo-Less Liposomal Formulation on Dietary Obesity-Related Metabolic Disorders in Mice.

Publications

Impact of A Cargo-Less Liposomal Formulation on Dietary Obesity-Related Metabolic Disorders in Mice.

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