Effects of a Whole Fruit–Rich Diet on Glycemic Control, Ectopic Fat, and Cardiovascular Risk Factors in Adults with Type 2 Diabetes

Introduction and Objective: Very-low-calorie diets and low-carbohydrate diets can improve glycemic control. However, less is known about the effects of carbohydrate-rich whole foods, such as whole fruit. Therefore, we performed the first clinical trial testing the effects of a whole fruit-rich diet on glycemic control, ectopic fat, and cardiovascular health in adults with type 2 diabetes (T2D). Methods: In this 12-week pilot study, 10 adults with insulin-independent T2D for ≤6 years progressively consumed more whole fruit during weeks 1-4 (ramp-up phase). During weeks 5-12, participants ate very large amounts of whole fruit (50% of energy intake, or ~16.4 servings/day) combined with a Mediterranean diet. Participants were kept weight stable. Outcomes were measured at weeks 0, 4, and 12. Glycemic control was assessed hierarchically by whether participants met the glycemic threshold for T2D remission, the total dosage of antihyperglycemic medications, an OGTT, and continuous glucose monitoring. Liver and pancreatic fat were assessed via MRI/S. BP and lipids were also measured. Results: The high-fruit diet improved glycemic control in 90% (9 of 10) of participants. Six out of 8 participants were weaned off their antihyperglycemic medications at week 10, and half of the weaned participants met the glycemic threshold for T2D remission at week 12 (p<0.0001). The whole fruit-rich diet also reduced the need for antihyperglycemic medications (p=0.03) and decreased systolic BP by 11 ± 2 mm Hg (p=0.0002). However, it increased triglycerides by 31 ± 15 mg/dl (p=0.04). There were no changes in liver fat (-1.3 ± 0.9%; p=0.14) or other outcomes. Intriguingly, mean 24-hour glucose and liver fat transiently increased and then decreased, potentially suggesting a period of metabolic adaptation. Conclusion: A high-fruit Mediterranean diet improves glycemic control, reduces the need for glucose-lowering medications, and lowers BP in people with early-stage T2D. Disclosure: C. Hanick: None. W. Garvey: Advisory Panel; Boehringer-Ingelheim, Eli Lilly and Company, Novo Nordisk, Fractyl Health, Inc., Alnylam Pharmaceuticals, Inc, Zealand Pharma A/S, Allurion, Carmot Therapeutics, Inc, TERNS Pharmaceuticals, Regeneron Pharmaceuticals, Inogen, Neurocrine, Keros Therapeutics. Research Support; Novo Nordisk, Eli Lilly and Company, Epitomee, Neurovalens, Roche Pharmaceuticals, Zealand Pharma A/S. A.M. Goss: None. J.S. Richman: None. K.J. Berg: None. C.M. Peterson: None. Funding: National Institute of Diabetes and Digestive and Kidney Diseases (P30 DK079626). NIH Predoctoral T32 Obesity Fellowship (T32 HL105349) from the National Heart, Lung, and Blood Institute.