Journal Name:
Am. J. Clin. Nutr.
Article Title:
Comparison of the effects on insulin resistance and glucose tolerance of 6-mo high-monounsaturated-fat, low-fat, and control diets.
Date Written:
2008
Volume:
87
Number:
4
Page:
855
Author(s):
Due, A.; Larsen, T.M.; Hermansen, K.; Stender, S.; Holst, J.J.; Toubro, S.; Martinussen, T.; Astrup, A.
Article:
The effect of dietary fat and carbohydrate on glucose metabolism has been debated for decades. Observational studies and intervention trials have shown that both the glycemic index (GI) of the diet and the amount and quality of fat in the diet are factors involved in the development of insulin resistance and type 2 diabetes. There is circumstantial evidence to suggest that a diet high in monounsaturated fat and a low GI could have a beneficial effect on type 2 diabetes. The intake of dietary fat, irrespective of its composition, has been associated with weight gain, but some studies indicate that the intake of unsaturated fat does not lead to the same weight gain as does an isocaloric saturated fat diet.
The purpose of the present study was to compare the effect on insulin resistance and glucose tolerance of 3 different ad libitum diets consumed in a 6-mo strictly controlled dietary intervention by healthy subjects after weight loss: a diet high in monounsaturated fat, a diet low in fat, or a control diet high in saturated fat.
Forty-six nondiabetic, obese [mean (+/-SEM) body mass index (in kg/m(2)): 31.2 +/- 0.3] men (n = 20) and premenopausal women (n = 26) aged 28.0 +/- 0.7 y were randomly assigned to 1 of 3 diets after > or = 8% weight loss: 1) MUFA diet (n = 16): moderate in fat (35-45% of energy) and high in monounsaturated fatty acids ( > 20% of energy); 2) LF diet (n = 18): low-fat diet (20-30% of energy), and 3) control diet (n = 12): 35% of energy as fat ( > 15% of energy as saturated fatty acids). Protein accounted for 15% of energy in all 3 diets. A 2-h oral-glucose-tolerance test (OGTT) was performed before and after the 6-mo dietary intervention.
After 6 months, the MUFA diet reduced fasting glucose (-3.0%), insulin (-9.4%), and the homeostasis model assessment of insulin resistance score (-12.1%). Compared with the MUFA diet, the control diet increased these variables [1.4%, 21.2%, and 22.8%, respectively], as did the LF diet [1.4%, 13.1%, and 15.5%, respectively]. In this weight-loss maintenance study, increases in fasting insulin and glucose concentrations along with slight weight regains with the LF and control diets were noted, whereas, despite a similar weight regain with the MUFA diet, reductions in fasting glucose and insulin concentrations were seen. A diet high in monounsaturated fat seems to have a beneficial effect on glucose metabolism independently of a small weight regain.
Previous research has found that an exchange of saturated for monounsaturated fat improved insulin sensitivity, whereas no improvement in fasting insulin or insulin secretion was seen. This may explain the lack of improvement in OGTT in the present trial, because the average fat intake in the MUFA group was 38.5%. A reduction in the total fat intake to 37% could possibly have resulted in a more pronounced beneficial effect of the MUFA diet on OGTT. The favorable effect of the MUFA diet on glucose metabolism may also have been due to a presumed lower glycemic load of the diet, because a low-GI diet stimulates lower insulin secretion and thereby potentially improves glucose metabolism. In the present study, the MUFA diet had a low GI and a low glycemic load because of its high content of unsaturated fat.
In conclusion, 6 month of a diet high in monounsaturated fat has a more favorable effect on glucose homeostasis than does the typical Western diet in the short term and may also be more beneficial than the official recommended low-fat diet during a period of weight regain subsequent to weight loss. The study participants in the present trial were young, normoglycemic, overweight or obese, and otherwise healthy, and the beneficial effect of the MUFA diet could be more pronounced in insulin-resistant subjects.
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