ArticleBMJ open diabetes research & care2016
Insulin resistance of protein anabolism accompanies that of glucose metabolism in lean, glucose-tolerant offspring of persons with type 2 diabetes.
Article in BMJ open diabetes research & care, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Defining Healthy Weight Loss and Target Weight in the Era of Highly Effective Treatment of Patients With Obesity.Journal of cachexia, sarcopenia and muscle · 2026Review
- Glucagon, Metabolic Dysfunction-Associated Steatotic Liver Disease and Amino Acids in Humans and Animals without Diabetes Mellitus-An Evidence Map.Life (Basel, Switzerland) · 2024Review
- Role of branched-chain amino acid metabolism in the pathogenesis of obesity and type 2 diabetes-related metabolic disturbances BCAA metabolism in type 2 diabetes.Nutrition & diabetes · 2022Review
- Molecular Mechanisms and Treatment of Sarcopenia in Liver Disease: A Review of Current Knowledge.International journal of molecular sciences · 2021Review
- Muscle and adipose tissue insulin resistance: malady without mechanism?Journal of lipid research · 2019Review
- Metformin inhibits proliferation and cytotoxicity and induces apoptosis via AMPK pathway in CD19-chimeric antigen receptor-modified T cells.OncoTargets and therapy · 2018Article
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Authors and funding
7 authors.
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Abstract
objectiveTo test whether protein anabolic resistance is an early defect in type 2 diabetes (T2D). RESEARCH DESIGN AND
methodsSeven lean, normoglycemic T2D offspring (T2D-O) and eight matched participants without family history (controls; C) underwent a 3-hour hyperinsulinemic (40 mU/m
resultsFasting 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.
conclusionsResistance 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.
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