PT  - JOURNAL ARTICLE
AU  - Sergio A Burgos
AU  - Vikram Chandurkar
AU  - Michael A Tsoukas
AU  - Stéphanie Chevalier
AU  - José A Morais
AU  - Marie Lamarche
AU  - Errol B Marliss
TI  - Insulin resistance of protein anabolism accompanies that of glucose metabolism in lean, glucose-tolerant offspring of persons with type 2 diabetes
AID  - 10.1136/bmjdrc-2016-000312
DP  - 2016 Nov 01
TA  - BMJ Open Diabetes Research & Care
PG  - e000312
VI  - 4
IP  - 1
4099  - http://drc.bmj.com/content/4/1/e000312.short
4100  - http://drc.bmj.com/content/4/1/e000312.full
SO  - BMJ Open Diab Res Care2016 Nov 01; 4
AB  - Objective To test whether protein anabolic resistance is an early defect in type 2 diabetes (T2D).Research design and methods Seven lean, normoglycemic T2D offspring (T2D-O) and eight matched participants without family history (controls; C) underwent a 3-hour hyperinsulinemic (40 mU/m2/min), euglycemic (5.5 mmol/L) and isoaminoacidemic clamp. Whole-body glucose and protein kinetics were measured with d-[3–3H]glucose and l-[l-13C]leucine, respectively. Plasma amino acids were measured by liquid chromatography-tandem mass spectrometry.Results Fasting glycemia and glucose kinetic variables did not differ between groups. Clamp decreases in glucose rate of appearance were not different, but rate of disappearance increased 29% less in T2D-O, to a significantly lower rate. Fasting leucine was higher in T2D-O, but kinetics did not differ. Clamp increases in leucine oxidation and decreases in endogenous rate of appearance (protein breakdown) were equal, but in T2D-O, non-oxidative rate of disappearance (protein synthesis) did not increase and net balance (synthesis—breakdown) did not become positive as in C.Conclusions Resistance of whole-body protein anabolism (synthesis and net balance) accompanies resistance of glucose uptake in T2D-O. Mechanisms responsible, possible roles in the increased risk of developing diabetes, and its potential impact on long-term protein balance require definition.