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the role of membrane rafts and caveolae, CD36 recycling between intracellular depots and the membrane, and chemical modifications of the protein that impact its turnover and recruitment).
Importantly, CD36 membrane levels and turnover are abnormal in diabetes, resulting in dysfunctional FA utilization.
From the 38 randomized patients, 20 opted to participate in the protein metabolism substudy, which happened simultaneously during the trial period.
Inclusion criteria included being on MHD for 6 months, well-functioning hemodialysis vascular access or permanent dialysis catheter, signs of chronic inflammation (average C-reactive protein [CRP] of ≥5 mg/L over three consecutive measurements), and acceptable dialysis adequacy (kt/V-3 fatty acids in MHD patients.Maintenance hemodialysis (MHD) patients are prone to have multiple catabolic processes that lead to a unique form of metabolic and nutritional derangement termed as protein energy wasting (PEW) of kidney disease (1,2).PEW is associated with major adverse clinical outcomes and is considered to be a significant comorbid condition leading to increased rates of hospitalization and death in patients undergoing MHD.The primary outcome was the change in forearm muscle protein breakdown measured at 12 weeks from baseline.Metabolic studies were performed on a nondialysis day and each metabolic study consisted of a 2-hour equilibration phase followed by a 1-hour sampling period (Figure 2).