Episode 27 - Adipocytes and insulin resistance

by Break Nutrition | Podcast

Show notes:

 

  • 60% of US adults are overweight to moderately obese but within that group there is great heterogeneity in their response to insulin ⇒ their degree of insulin sensitivity can vary more than sixfold at any given BMI within this range
  • Adults constantly form and replace adipose cells, called turnover
  • 2 places to measure fat are the femoral (leg fat) and subcutaneous (under your skin and predominantly white) adipose tissues
  • For IMGU (insulin mediated glucose uptake), the higher the SSPG (steady-state plasma glucose) concentration, the more IR the individual
  • Insulin sensitive people have
    • larger adipose cells
    • more (functional) small adipose cells
    • decreased expression of adipocyte-differentiation genes
  • A clue from animal lipodystrophy models about how insulin resistance manifests is that the absence of subcutaneous fat is associated with ectopic fat and severe insulin resistance

 

  • Adipose Cell Size and Regional Fat Deposition as Predictors of Metabolic Response to Overfeeding in Insulin-Resistant and Insulin-Sensitive Humans (McLaughlin et al. 2016)
    • The study select for “overweight-to-moderately obese individuals classified as IS or IR”
    • SSPG assays were use to exclude moderately IS/IR people, leaving only the IS or IR
    • This was an overfeeding study by a whopping 880 kcals per day. This was so that “adipose cells would be near or at maximal storage capacity and would likely exhibit differential adipose cell and tissue responses to additional TG storage demands”
      • The overfeeding diet was 43% carbohydrate, 42% fat, and 15% protein
    • Prediction about the IS subjects ⇒ “due to enhanced ability to differentiate and recruit new adipose cells, would be protected from adipocyte hypertrophy, ectopic fat deposition, lipolysis, and/or worsening of insulin resistance”
    • Prediction about the the IR subjects⇒ “impaired adipocyte differentiation and TG storage, including adipocyte hypertrophy, lipolysis/increased circulating free fatty acid (FFA), fat deposition in visceral and intrahepatic depots, and worsening insulin resistance”
    • Results about the IR subjects
      • Correct “significantly larger peak diameter of fat cells” (hypertrophy)
      • Correct “greater percentage of small cells than the IS subjects” (adipocyte-specific hyperplasia)
      • Correct “VAT and %VAT were significantly greater in the IR subgroup” (visceral fat increased)
      • Correct “IHL was nearly eightfold greater” (liver fat increased)
      • “IR increased significantly in both groups (45% in the IS and 8% in the IR group)” ⇒ there was significantly more IR proportionally speaking in the insulin SENSITIVE group !
      • “The peak diameter increased in both groups, but this change was only statistically significant in the IS group”
      • In contrast to our hypothesis that IS subjects would demonstrate adaptive adipose tissue and metabolic responses to weight gain, we found the opposite: IS subjects exhibited maladaptive adipose tissue responses and developed clinically significant insulin resistance
      • Worsening metabolic response “were independent of weight gain per se, implying that differential cellular and regional fat distribution patterns of adipose tissue may contribute to the metabolic heterogeneity of obesity
      • The authors noted a “paradox: although the IS subjects had a healthier adipose and metabolic profile at baseline, with the exception of TG and VLDL cholesterol, they decompensated to a greater degree with weight gain” ⇒ this remains hard to explain.

 

  • Association of in vivo adipose tissue cellular kinetics with markers of metabolic health in humans (White et al. 2017)
    • AT expandability hypothesis ⇒ a lack of hyperplasia results in the limited capacity of AT to expand and store fat, causing metabolic derangements

This study found that no, it is in fact “hyperplastic expansion , that is associated with metabolic syndrome”

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