Research

Hormonal

Germline loss-of-function PTEN mutations cause constitutive insulin sensitivity, resulting in significantly lower fasting insulin levels and higher glucose disposal rates despite the presence of obesity.

This finding highlights that metabolic health (insulin sensitivity) is genetically regulated and can be preserved in obesity if specific pathways (like PTEN) are active. It suggests that BMI alone is an insufficient predictor of metabolic risk for all individuals, particularly those with specific genetic profiles.

GoodSupportsHIGH confidence
Measures of insulin resistance were lower in the patients with a PTEN mutation than in controls (e.g., mean fasting plasma insulin level, 29 pmol per liter [range, 9 to 99] vs. 74 pmol per liter [range, 22 to 185]; P = 0.001). This finding was confirmed with the use of hyperinsulinemic euglycemic clamping, showing a glucose infusion rate among carriers 2 times that among controls (P = 0.009).
Aparna Pal et al. · New England Journal of Medicine · 2012

Why this rating

Small sample size (n=15) but high-quality measurement methods (hyperinsulinemic euglycemic clamp) and strong statistical significance.

Source

<i>PTEN</i> Mutations as a Cause of Constitutive Insulin Sensitivity and Obesity

Aparna Pal et al. · New England Journal of Medicine · 2012

DOI 10.1056/nejmoa1113966

cohort · n=2112Cited 232×
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DOI resolved against Crossref · corpus check 2026-06-10

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