The Journal of Japan Atherosclerosis Society
Online ISSN : 2185-8284
Print ISSN : 0386-2682
ISSN-L : 0386-2682
Glucose Intolerance and Hyperinsulinemia in Familial Combined Hyperlipidemia
Junji KOIZUMITakahiro HORITATadayoshi TAKEGOSHIHiroshi MABUCHI
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JOURNAL OPEN ACCESS

1996 Volume 24 Issue 3 Pages 133-139

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Abstract
Familial combined hyperlipidemia (FCHL) is a common genetic hyperlipidemia, and has been known to cause premature coronary heart disease (CHD). The impaired glucose tolerance with hyperinsulinemia also is a potent risk factor for CHD. Familial hyperlipidemia and hyperinsulinemia in diabetic patients, may be important elements linkaging diabetes and CHD. In the present study, insulin responses after 75g glucose administration in non-obese FCHL patients (BMI<25, FCHL group, n=20), were compared with those in familial hypercholesterolemic (FH group, n=49) or normolipidemic patients (Control group, n=41). The patients were divided to the normal, impaired and diabetic glucose tolerance groups according to the WHO criteria.
Seven FCHL patients (35%) showed an impaired glucose tolerance and 5 FCHL patients (25%) diabetic glucose tolerance. Fasting plasma glucose levels and area under the plasma glucose concentration-time curve showed no differences among FCHL, FH and control groups in each normal, impaired and diabetic glucose tolerance group. However, the FCHL patients with normal glucose tolerance had a significant higher level of plasma insulin 60 minute after glucose administration than the FH and control groups (p<0.05), and the FCHL patients with impaired glucose tolerance a significant higher level of plasma insulin 30 and 120 minute after glucose administration than FH and control groups (p<0.05). Area under the plasma insulin concentration-time curve (AUC-IRI) in the FCHL patients with normal and impaired glucose tolerances were 162±42μU/ml/h and 208±60μU/ml/h, respectively, which were significant higher than those in the control group (77±6μU/ml/h and 103±18μU/ml/h)(p<0.05). There were significant relationships between AUC-IRI and LDL-cholesterol levels in FCHL patients (p<0.05), but no relationships between serum triglyceride or HDL-cholesterol levels, and AUC-IRI.
In conclusion, FCHL patients showed hyperinsulinemia after glucose administration, and may contribute to the increased CHD in the patients with glucose intolerance, according to the similar manner to the insulin resistance syndrome. Therefore, FCHL should be considered in the pathogenesis of CHD in the diabetic patients with hyperlipidemia, hyperinsulinemia and CHD.
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