The relationship of fasting hyperglycemia to changes in fat and muscle mass after exercise training in type 2 diabetes

Abstract

Aims Exercise training (ET) has been variably associated with body composition changes among persons with type 2 diabetes (T2DM). The degree to which these changes are related to hyperglycemia remains unclear. Our objective was to investigate the relationship of baseline fasting glucose (FG) to the magnitude of muscle gains and fat loss after ET in individuals with T2DM. Methods Participants were enrolled in the SHAPE-2 trial, a six month supervised aerobic and resistance training intervention (three days/week), at Johns Hopkins. This was a post-hoc single arm intervention study of participants who completed the exercise intervention (n=50). Participants were aged 40-65 years and had T2DM that was not treated with insulin. Body composition was assessed by DEXA. Results After 6 months of ET, total fat mass decreased (−2.1 ± 3.1 kg) and total lean body mass (LBM) increased (0.5 ± 2.0 kg) overall, but there was variability among individual participants. There was an increase in % total LBM (1.4 ± 1.9%) and decrease in % total body fat mass (−1.5±2.0%) after ET. Interestingly, each standard deviation (SD) increase in baseline FG (mean=135.5 mg/dl; SD= 39.0 mg/dl) was related to a significant increase in % total LBM (0.54±0.26%, p=0.048) and decrease in % total body fat (−0.57±0.27%, p=0.04) after ET among individual participants. Conclusions Our data demonstrate that muscle gains and fat loss after ET are positively related to baseline hyperglycemia. Further studies are needed to characterize differences in metabolic response following ET among persons with diabetes.

Age-dependent insulin resistance in male mice with null deletion of the carcinoembryonic antigen-related cell adhesion molecule 2 gene

“…As in other murine models of altered metabolism [30, 31], this could contribute to insulin resistance in skeletal muscle, as manifested by glucose intolerance and underlined by reduced insulin-stimulated Akt phosphorylation, a key mediator of glucose uptake [32]. Glucose uptake in skeletal muscle becomes limited in parallel to an age-dependent reduction in metabolically active lean mass and an increase in visceral obesity [33]. Consistent with this, lean mass decreased reciprocally to the increase in fat mass in older Cc2 −/− male mice.…”

“…Whereas age-related hyperinsulinaemia, insulin resistance and visceral obesity [41–43] are commonly associated with reduced glucose uptake in skeletal muscle in parallel with a reduction in metabolically active lean mass [33], decreased fenestration in the liver sinusoidal endothelium and other structural changes that reduce insulin uptake by hepatocytes, and hence reduce insulin clearance, have recently emerged as mechanisms underlying age-related hyperinsulinaemia and insulin resistance [44]. The current study provides an alternative mechanism of hyperinsulinaemia in older Cc2 −/− male mutant mice, implicating a progressive reduction in hepatic CEACAM1-mediated insulin clearance that fails to counter persistent GLP-1-mediated release of insulin in older mutant mice.…”

Resistance and Aerobic Training in the Treatment of Type 2 Diabetes Mellitus

“…After AE and RT interventions, participants presented total fat mass decreased and total lean body mass increased in association of fasting glucose reduction. So, these data demonstrate that muscle gain and fat loss after ET are positively related to baseline hyperglycemia [20].…”

“…However, [19] highlighted some limitations, as sample size and subjectivity on physical function measurement [19]. In a contribution to this findings, [20] performed supervised aerobic and resistance training intervention for 6 months in 50 individuals with DM2. After AE and RT interventions, participants presented total fat mass decreased and total lean body mass increased in association of fasting glucose reduction.…”

Does lean body mass equal health despite body mass index?

“…5 Lean body mass is the primary site of glucose uptake 8 ; and therefore, it has been suggested that LBM protects against cardio-metabolic risk factors and diabetes. 9,10 Although rational, few studies support that both BMI and high-LBM are independently associated with unfavorable cardio-metabolic profiles. 5,11 For example, a study including 421 men and women suggests that age and LBM (but not fat mass) explained 46% of the unfavorable cardio-metabolic risk factors profile.…”