Abstract
Although low-calorie diets (LCD) improve glucose regulation, it is unclear if interval exercise (INT) is additive. We examined the impact of an LCD versus LCD + INT training on ß-cell function in relation to glucose tolerance in obese adults. Twenty-six adults (Age: 46 ± 12 year; BMI 38 ± 6 kg/m2) were randomized to 2-week of LCD (~1200 kcal/day) or energy-matched LCD + INT (60 min/day alternating 3 min at 90 and 50% HRpeak). A 2 h 75 g oral glucose tolerance test (OGTT) was performed. Insulin secretion rates (ISR) were determined by deconvolution modeling to assess glucose-stimulated insulin secretion ([GSIS: ISR/glucose total area under the curve (tAUC)]) and ß-cell function (Disposition Index [DI: GSIS/IR]) relative to skeletal muscle (Matsuda Index), hepatic (HOMA-IR) and adipose (Adipose-IRfasting) insulin resistance (IR). LCD + INT, but not LCD alone, reduced glucose and total-phase ISR tAUC (Interactions: p = 0.04 and p = 0.05, respectively). Both interventions improved skeletal muscle IR by 16% (p = 0.04) and skeletal muscle and hepatic DI (Time: p < 0.05). Improved skeletal muscle DI was associated with lower glucose tAUC (r = −0.57, p < 0.01). Thus, LCD + INT improved glucose tolerance more than LCD in obese adults, and these findings relate to ß-cell function. These data support LCD + INT for preserving pancreatic function for type 2 diabetes prevention.
Highlights
Obesity affects about 13% of adults worldwide and increases the risk for type 2 diabetes (T2D) [1,2]
Neither intervention altered body fat % (Time: p = 0.46), fat-free mass (FFM) increased slightly after Low-calorie diet (LCD) + interval exercise (INT) when compared with LCD
The major finding of the present study was that 2 weeks of an LCD combined with INT reduced glucose and Insulin secretion rates (ISR) tAUC responses to an oral glucose tolerance test (OGTT) compared to a LCD alone (Figure 1)
Summary
Obesity affects about 13% of adults worldwide and increases the risk for type 2 diabetes (T2D) [1,2]. While the relation between excess body fat and T2D is complex, the development of T2D is mainly characterized by insulin resistance that contributes to hyperinsulinemia and pancreatic ß-cell dysfunction [3,4]. Over time, it is the loss of ß-cell function that leads to impaired glucose tolerance and T2D [3,5]. The oral disposition index (DI) is a measure of pancreatic insulin secretion [6,7] and is a stronger predictor of future T2D risk than insulin sensitivity alone [8]. Interventions that improve pancreatic ß-cell dysfunction are essential to the prevention of T2D [9].
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