Insulin Resistance Assay for Microbiome-host Interactions
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Overview
Insulin is the most potent anabolic hormone known and is essential for proper tissue development, growth, and maintenance of whole-body glucose homeostasis. Insulin also profoundly affects lipid metabolism, increasing lipid synthesis in the liver and adipocytes and reducing fatty acids released from triglycerides in fat and muscle. Obesity and diabetes are two metabolic disorders linked to an inflammatory process called insulin resistance. Insulin resistance is a pathological condition of declined cellular response to insulin causing hyperglycemia, despite β-cells of the pancreas being able to produce enough insulin.
Probiotics Improve Insulin Resistance
Probiotics may represent a therapeutic tool to attenuate the microbial-related mechanisms that produce insulin resistance in human diseases. Probiotic supplementation has been studied to reduce the expression of NOD1 and PRR genes in obese mice causing a reduction in weight gain and insulin resistance. The protein kinases JNK and inhibitors of kappa B kinase (IKK) responsible for inflammation and insulin resistance are also downregulated by probiotic supplementation. Probiotic supplementations reduce TLR signaling pathway, and NFκB translocation into the nucleus and thus reduce inflammation and insulin resistance.
Fig.1 Effects of probiotic administration on obesity-related features by changes in the gut microbiota profile. (Bagarolli, 2017)
Molecular Targets of Insulin Resistance
TNF-α is known to contribute to insulin resistance both through activation of mitogen-activated protein kinase (MAPK) and IKK resulting in serine phosphorylation of IRS-1 and through activation of protein tyrosine phosphorylase b which leads to dephosphorylation and inactivation of the insulin receptor and IRS-1. Indirectly, TNF-α can also increase hepatic triglyceride release, thereby contributing to abnormal fatty acid accumulation in skeletal muscle. Many different altered metabolic states, such as persistent elevation of circulating glucose, insulin, fatty acids, and cytokines, can lead to peripheral insulin resistance. The molecular targets and intracellular signaling systems modified during insulin resistance have attracted much attention.
Fig.2 Schematic model indicating the presence of two potential insulin receptor-dependent signal transduction pathways. (Pessin, 2000)
Insulin Resistance Assay at Creative Biolabs
TNF-α has been implicated as a causative factor in the pathogenesis of obesity-related insulin resistance and type 2 diabetes mellitus. Thus, the present evidence suggests that exogenous TNF-α induces insulin resistance in animals, whereas neutralization of TNF-α enhances insulin sensitivity. The inflammation-induced insulin resistance model recreates the interplay between adipocytes, which become insulin resistant after treatment with TNF-α, and the functionality of the epithelial cell layer (Caco-2 cells). Cultured 3T3-L1 adipocytes have been widely used in studies of insulin signaling and glucose transport. In this assay, the direct or indirect ability of products administered to the gut (colonic simulation or upper gastrointestinal simulation) to reduce insulin resistance could be investigated.
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References
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Bagarolli, R.A.; et al. Probiotics modulate gut microbiota and improve insulin sensitivity in diet-induced-obese mice. J Nutr Biochem. 2017, 50: 16-25.
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Pessin, J.E.; Saltiel, A.R. Signaling pathways in insulin action: molecular targets of insulin resistance. J Clin Invest. 2000, 106: 165-9.
For Research Use Only. Not intended for use in food manufacturing or medical procedures (diagnostics or therapeutics). Do Not Use in Humans.
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