Episode 5 of the Break Nutrition Show Gabor and I  had a discussion about the paper called “Lipid-overloaded enlarged adipocytes provoke insulin resistance independent of inflammation”, covering the following points (and more):

Link: http://www.ncbi.nlm.nih.gov/pubmed/25733684

• The concept of IR occurring after the lipid-derived enlargement of adipocytes (as opposed to the other model of IR preceding it)
• The difference in mild/early-stage obesity versus severe/late-stage obesity
• Mechanisms whereby adipocyte-focused inflammation appears necessary to make adipocytes more insulin resistance in severe/late-stage obesity but not in mild/early-stage obesity (within this human in vitro and in vivo rodent model)
• How MUFAs and especially SFAs challenged adipocytes become enlarged
• How inflammation occurs with MUFAs challenged adipocytes but not with SFAs challenged ones
• Why the study devised 4 categories for the adipocytes; (1) small ones with small droplets (2) large ones with small droplets (3) small ones with a few large single-like droplets (4) large ones with a few large single-like droplets
• Why the 4th kind of adipocyte, a large one with a few large single-like droplets, is the most pathological kind (see following point)
• How the cortactin and filamentous cytoskeleton of adipocytes become disorganized when the adipocyte is sufficiently enlarged and thus (partially) inhibiting GLUT4’s transport and expression at the plasma membrane
• How proper GLUT4 expression in adipocytes helps maintain insulin sensitivity, proper hypertrophy (volume) and hyperplasia (adipocyte numbers)
• Lastly, how the first effects of the immune system on the adipocyte is to remodel it rather than induce insulin resistance, typical of mild/early-stage obesity…and how inflamed adipose tissue typical of severe/late-stage obesity contributes to systemic insulin resistance.

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