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Overall, multiple mechanisms including inflammation and reduced FA re-esterification likely explain the impaired buffering capacity in adipocytes during obesity that leads to the spillover of FAs, buildup of toxic lipid metabolites and allosteric regulators that suppress insulin action and increased hepatic glucose output, respectively (Figure 5)

High activity of NNMT is also correlated with lower levels of glucose transporter 4 (GLUT4), which is vital for glucose uptake from the bloodstream into fat and muscle cells

Stubborn fat that does not respond to diet and exercise is often a metabolic problem, not a willpower problem

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For laboratories investigating the downstream growth factor signalling pathway separately, our IGF-1 LR3 research guide provides detailed information on how IGF-1 LR3 is used to study growth factor receptor biology in controlled research settings