Skeletal Muscle Protein Anabolic Response to Increased Energy and Insulin Is Preserved in Poorly Controlled Type 2 Diabetes

摘要: Individuals with type 2 diabetes (T2DM)4 are characterized by hyperinsulinemia and insulin resistance leading to fasting postprandial hyperglycemia abnormal fatty acid metabolism (1,2). In addition, T2DM is associated metabolic abnormalities in glucose utilization, including impaired tolerance (3,4) that might also extend muscle protein if signaling compromised (5). Although a potent stimulator of skeletal anabolism, the specific mechanism which exerts its effects human controversial. For example, several studies have reported an inhibitory effect on breakdown (6–10), whereas others shown direct stimulatory synthesis (11–14). The importance regulating turnover highlighted estimated contribution (30–50%) whole body (6,15). Furthermore, energy-requiring process, when additional energy supplied form either or lipids, rate subsequently reduced (16–20). However, interaction between increase nutritional has not been well described. Few addressed amino kinetics T2DM. Most resistant obese individuals (21–25). it whole-body proteolysis significantly elevated obesity (26,27). There even fewer looked at utilization muscle. Using arteriovenous two-pool model calculate labeled phenylalanine across leg, one study found that, though was T2DM, release leg (an index proteolysis) (15). recent reports no differences fractional synthetic rates group healthy controls (24). traditional model, often used actually measures net plasma acids while offering any insight into intracellular kinetics. Therefore, remains unclear whether present state T2DM. The first aim this determine poorly controlled (i.e., hemoglobin A1c > 7%) affects postabsorptive anabolism. Our second hyperinsulinemia, combination high availability, stimulates anabolism same extent as controls. To address our aims we studied regional following overnight fast during hyperinsulinemic-isoenergetic clamp subjects