Effect of source of dietary fats on serum glucose, insulin, and gastric inhibitory polypeptide responses to mixed test meals in subjects with non-insulin dependent diabetes mellitus

• Published in: Journal of the American College of Nutrition Vol. 7; no. 2; p. 129
• Main Authors: Lardinois, C K, Starich, G H, Mazzaferri, E L, DeLett, A
• Format: Journal Article
• Language: English
• Published: United States 01.04.1988
• Subjects: Adult; Aged; Blood Glucose - metabolism; C-Peptide - blood; Diabetes Mellitus, Type 2 - blood; Dietary Fats - administration & dosage; Dietary Fats, Unsaturated - administration & dosage; Female; Gastric Inhibitory Polypeptide - blood; Humans; Insulin - blood; Male; Middle Aged
• ISSN: 0731-5724
• DOI: 10.1080/07315724.1988.10720229

We recently demonstrated that normal subjects given mixed test meals of varying fatty acid composition showed significantly greater serum insulin responses to meals enriched with polyunsaturated fat as compared to those in which the fat content was derived from saturated fatty acids. To determine if a similar phenomenon occurs in subjects with non-insulin dependent diabetes mellitus (NIDDM), serum glucose, insulin, C-peptide, and gastric inhibitory polypeptide (GIP) responses to three mixed test meals of varying fatty acid composition were assessed in twelve subjects with NIDDM. Baseline means (+/- SEM) fasting serum glucose concentration was 205 +/- 15 mg/dl and mean glycosylated hemoglobin was 8.5 +/- 0.5%. Fatty acids in the test meals were either saturated fats, or polyunsaturated fats derived from vegetables or fish. Each test meal provided 40% of the subjects' calculated daily caloric requirement and contained approximately 45% carbohydrate, 40% fat, and 15% protein. No appreciable differences in serum glucose, insulin, and C-peptide responses occurred during the three mixed test meals. Although GIP values were higher in the saturated fat and the vegetable meals when compared to the fish meal, the differences did not reach statistical significance. The inability of NIDDM subjects to evoke a greater insulin response to polyunsaturated fatty acids than to saturated fatty acids suggests another pathogenetic factor contributing to their glucose intolerance.