Plain language summary
The development of type 2 diabetes is characterised by insulin resistance and dysfunction of the pancreas. Over time, loss of function of the ß-cells of the pancreas leads to impaired tolerance of blood sugar and type 2 diabetes. Low-calorie diets have been shown to improve blood sugar regulation, but it is unclear what impact interval exercise has in addition to a low-calorie diet. This study tested the hypothesis that combining interval exercise with a low-calorie diet would enhance pancreatic function compared to a low calorie diet alone in adults with obesity. Twenty-six obese adults were assigned to 2 weeks of a LCD (1200 kcal/day), using meal replacement shakes for breakfast and lunch. Half the group also underwent 60 minutes of interval training a day; after each session they received a 350 kcal shake to compensate for the calories burned during training. A series of blood tests was carried out to measure glucose tolerance and insulin secretion rates. Combining a low calorie diet with interval training reduced glucose and insulin secretion rates, whereas the low calorie diet alone did not. Both interventions improved insulin sensitivity. The authors concluded that the data supports combining low calorie diets with interval training to preserve pancreatic function and prevent type 2 diabetes.
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.
Methodological quality
Allocation concealment
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No
