Abstract
The aim of this study was to test the effect of a plant-based dietary intervention on beta-cell function in overweight adults with no history of diabetes. Participants (n = 75) were randomized to follow a low-fat plant-based diet (n = 38) or to make no diet changes (n = 37) for 16 weeks. At baseline and 16 weeks, beta-cell function was quantified with a mathematical model. Using a standard meal test, insulin secretory rate was calculated by C-peptide deconvolution. The Homeostasis Model Assessment (HOMA-IR) index was used to assess insulin resistance while fasting. A marked increase in meal-stimulated insulin secretion was observed in the intervention group compared with controls (interaction between group and time, Gxt, p < 0.001). HOMA-IR index fell significantly (p < 0.001) in the intervention group (treatment effect −1.0 (95% CI, −1.2 to −0.8); Gxt, p = 0.004). Changes in HOMA-IR correlated positively with changes in body mass index (BMI) and visceral fat volume (r = 0.34; p = 0.009 and r = 0.42; p = 0.001, respectively). The latter remained significant after adjustment for changes in BMI (r = 0.41; p = 0.002). Changes in glucose-induced insulin secretion correlated negatively with BMI changes (r = −0.25; p = 0.04), but not with changes in visceral fat. Beta-cell function and insulin sensitivity were significantly improved through a low-fat plant-based diet in overweight adults.
Highlights
Impairment of pancreatic beta-cell function, typically preceded by insulin resistance in muscle and liver cells, is a key factor in type 2 diabetes [1]
The aim of this study was to test the effect of a dietary intervention on beta-cell function and insulin resistance in overweight adults with no history of diabetes
“normalized” for plasma glucose levels) did not improve. This physiologic reaction of beta-cells to compensate for impaired glycemic control, together with insulin resistance, which had a tendency to increase in controls, are two main pathophysiologic mechanisms in development of beta-cell dysfunction, and eventually diabetes [1], with reduced beta-cell function playing the decisive role [3]
Summary
Impairment of pancreatic beta-cell function, typically preceded by insulin resistance in muscle and liver cells, is a key factor in type 2 diabetes [1]. Improvements in beta-cell function, are not typically a goal of diabetes treatment. Beta-cell failure reflects a relative loss of beta-cell mass due to apoptosis [2], as well as selective loss of sensitivity to glucose, along with the loss of first-phase insulin secretion [3]. Limited data suggest that beta-cell function and beta-cell mass may be influenced by diet [4,5,6] and physical activity [4]
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