A high-fat meal increases the postprandial glucose levels and insulin requirements of patients with type 1 diabetes, according to research published online Nov. 27 in Diabetes Care.
Howard A. Wolpert, M.D., of the Joslin Diabetes Center in Boston, and colleagues conducted a crossover study that compared glucose control during two 18-hour periods after either a high-fat dinner (60 g) or a low-fat dinner (10 g) with identical carbohydrate and protein content. The protocol was completed by seven patients with type 1 diabetes.
Although considerable interindividual differences were noted, the researchers found that significantly more insulin units were required after a high-fat rather than low-fat dinner (12.6 ± 1.9 units versus 9.0 ± 1.3 units). However, even with additional insulin units, the high-fat meal caused more hyperglycemia. For a high-fat dinner, the carbohydrate-to-insulin ratio was significantly lower.
”The evidence from this study that dietary fat can cause postprandial hyperglycemia in some individuals with type 1 diabetes highlights the limitations of the current carbohydrate-based approach to bolus dose calculation that is widely used in intensive diabetes management,” the authors write. ”Further studies are needed to develop and validate alternative insulin dosing algorithms for higher-fat meals, and to define new nutritional approaches for minimizing hyperglycemia induced by dietary fat.”
Abstract
Dietary Fat Acutely Increases Glucose Concentrations and Insulin Requirements in Patients With Type 1 Diabetes
Implications for carbohydrate-based bolus dose calculation and intensive diabetes management
Howard A. Wolpert, MD1,2⇓,
Astrid Atakov-Castillo, BA1,
Stephanie A. Smith, MPH1 and
Garry M. Steil, PHD2,3
+ Author Affiliations
1Joslin Diabetes Center, Boston, Massachusetts
2Harvard Medical School, Boston, Massachusetts
3Children’s Hospital, Boston, Massachusetts
Abstract
OBJECTIVE Current guidelines for intensive treatment of type 1diabetes base the mealtime insulin bolus calculation exclusively on carbohydrate counting. There is strong evidence that free fatty acids impair insulin sensitivity. We hypothesized that patients with type 1 diabetes would require more insulin coverage for higher-fat meals than lower-fat meals with identical carbohydrate content.
RESEARCH DESIGN AND METHODS We used a crossover design comparing two 18-h periods of closed-loop glucose control after high-fat (HF) dinner compared with low-fat (LF) dinner. Each dinner had identical carbohydrate and protein content, but different fat content (60 vs. 10 g).
RESULTS Seven patients with type 1 diabetes (age, 55 ± 12 years; A1C 7.2 ± 0.8%) successfully completed the protocol. HF dinner required more insulin than LF dinner (12.6 ± 1.9 units vs. 9.0 ± 1.3 units; P = 0.01) and, despite the additional insulin, caused more hyperglycemia (area under the curve >120 mg/dL = 16,967 ± 2,778 vs. 8,350 ± 1,907 mg/dL⋅min; P < 0001). Carbohydrate-to-insulin ratio for HF dinner was significantly lower (9 ± 2 vs. 13 ± 3 g/unit; P = 0.01). There were marked interindividual differences in the effect of dietary fat on insulin requirements (percent increase significantly correlated with daily insulin requirement; R2 = 0.64; P = 0.03).
CONCLUSION This evidence that dietary fat increases glucose levels and insulin requirements highlights the limitations of the current carbohydrate-based approach to bolus dose calculation. These findings point to the need for alternative insulin dosing algorithms for higher-fat meals and suggest that dietary fat intake is an important nutritional consideration for glycemic control in individuals with type 1 diabetes.
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