Gröntvedt
2008-09-17, 01:08
ABSTRACT
Background: Exaggerated and prolonged postprandial triglyceride
concentrations are associated with numerous conditions related to
insulin resistance, including obesity, type 2 diabetes, and the metabolic
syndrome. Although dietary fats profoundly affect postprandial
hypertriglyceridemia, limited data exist regarding their effects
on postprandial glucose homeostasis.
Objective: We sought to determine whether postprandial glucose
homeostasis is modulated distinctly by high-fat meals enriched in
saturated fatty acids (SFAs) or monounsaturated fatty acids
(MUFAs).
Design: Normotriglyceridemic subjects with normal fasting glucose
and normal glucose tolerance were studied. Blood samples were
collected over the 8 h after ingestion of a glucose and triglyceride
tolerance test meal (GTTTM) in which a panel of dietary fats with a
gradual change in the ratio of MUFAs to SFAs was included. On 5
separate occasions, basal and postprandial concentrations of glucose,
insulin, triglyceride, and free fatty acids (FFAs) were measured.
Results: High-fat meals increased the postprandial concentrations
of insulin, triglycerides, and FFAs, and they enhanced postprandial
cell function while decreasing insulin sensitivity (as assessed with
different model-based and empirical indexes: insulinogenic index,
insulinogenic index/homeostasis model assessment of insulin resistance,
area under the curve for insulin/area under the curve for
glucose, homeostasis model assessment for cell function, and
GTTTM-determined insulin sensitivity, oral glucose insulin sensitivity,
and the postprandial Belfiore indexes for glycemia and blood
FFAs. These effects were significantly ameliorated, in a direct linear
relation, when MUFAs were substituted for SFAs.
Conclusions: The data presented here suggest that cell function
and insulin sensitivity progressively improve in the postprandial
state as the proportion ofMUFAswith respect to SFAs in dietary fats
increases. Am J Clin Nutr 2008;88:638–44
Background: Exaggerated and prolonged postprandial triglyceride
concentrations are associated with numerous conditions related to
insulin resistance, including obesity, type 2 diabetes, and the metabolic
syndrome. Although dietary fats profoundly affect postprandial
hypertriglyceridemia, limited data exist regarding their effects
on postprandial glucose homeostasis.
Objective: We sought to determine whether postprandial glucose
homeostasis is modulated distinctly by high-fat meals enriched in
saturated fatty acids (SFAs) or monounsaturated fatty acids
(MUFAs).
Design: Normotriglyceridemic subjects with normal fasting glucose
and normal glucose tolerance were studied. Blood samples were
collected over the 8 h after ingestion of a glucose and triglyceride
tolerance test meal (GTTTM) in which a panel of dietary fats with a
gradual change in the ratio of MUFAs to SFAs was included. On 5
separate occasions, basal and postprandial concentrations of glucose,
insulin, triglyceride, and free fatty acids (FFAs) were measured.
Results: High-fat meals increased the postprandial concentrations
of insulin, triglycerides, and FFAs, and they enhanced postprandial
cell function while decreasing insulin sensitivity (as assessed with
different model-based and empirical indexes: insulinogenic index,
insulinogenic index/homeostasis model assessment of insulin resistance,
area under the curve for insulin/area under the curve for
glucose, homeostasis model assessment for cell function, and
GTTTM-determined insulin sensitivity, oral glucose insulin sensitivity,
and the postprandial Belfiore indexes for glycemia and blood
FFAs. These effects were significantly ameliorated, in a direct linear
relation, when MUFAs were substituted for SFAs.
Conclusions: The data presented here suggest that cell function
and insulin sensitivity progressively improve in the postprandial
state as the proportion ofMUFAswith respect to SFAs in dietary fats
increases. Am J Clin Nutr 2008;88:638–44