Effects of bezafibrate on insulin sensitivity and insulin secretion in non-obese Japanese type 2 diabetic patients

被引:57
作者
Taniguchi, A
Fukushima, M
Sakai, M
Tokuyama, K
Nagata, I
Fukunaga, A
Kishimoto, H
Doi, K
Yamashita, Y
Matsuura, T
Kitatani, N
Okumura, T
Nagasaka, S
Nakaishi, S
Nakai, Y
机构
[1] Kansai Denryoku Hosp, Div Diabet, Osaka, Japan
[2] Kyoto Univ, Grad Sch Med, Dept Metab & Clin Nutr, Kyoto, Japan
[3] Univ Tsukuba, Inst Hlth & Sports Sci, Lab Biochem Exercise & Nutr, Tsukuba, Ibaraki 305, Japan
[4] Kyoto Univ, Grad Sch Med, Kansai Hlth Management Ctr, Osaka, Japan
[5] Jichi Med Sch, Div Endocrinol & Metab, Minami Kawachi, Tochigi, Japan
[6] Kyoto Univ, Coll Med Technol, Div Sci Nursing, Kyoto, Japan
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2001年 / 50卷 / 04期
关键词
D O I
10.1053/meta.2001.21028
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The aim of the present study was to investigate the effect of bezafibrate on insulin sensitivity and insulin secretion in 30 non-obese Japanese type 2 diabetic patients with hypertriglyceridemia (serum triglycerides > 150 mg/dL). Insulin sensitivity was measured with homeostasis model assessment insulin resistance (HOMA-IR) proposed by Matthews et at. HOMA-B-cell function, proposed by Matthews et al validated against minimal model-derived insulin secretion, was used to assess pancreatic insulin function. Twenty-two patients were treated with glibenclimide and the rest were treated with diet alone. All patients were treated with bezafibrate (400 mg/d) for 3 months. There were no changes in diet and the dose of any medications used throughout the study. Fasting glucose, insulin, triglycerides, HDL cholesterol, and total cholesterol levels were measured before and after treatment of bezafibrate. After treatment of bezafibrate for 3 months, serum triglyceride levels significantly decreased from 277 +/- 30 to 139 +/- 9 mg/dL (P < .001) and serum HDL cholesterol levels increased significantly from 45 <plus/minus> 2 to 52 +/- 2 mg/dL (P = .003). Serum cholesterol level was unchanged during the study (198 +/- 7 v 201 +/- 7 mg/dL, P = .383). Fasting glucose (163 +/- 8 v 139 +/- 6 mg/dL, P = .006) significantly decreased after the treatment with bezafibrate. HbA1c levels decreased, although not statistically significant (7.50 +/- 0.25 v 7.17% +/- 0.19%, P = .147). On the other hand, fasting insulin (9.3 +/- 0.7 v 7.3 +/- 0.5 muU/mL, P = .010) and HOMA-IR (3.61 +/- 0.24 to 2.53 +/- 0.20, P < .001) levels decreased significantly after the treatment with bezafibrate. In contrast, HOMA-B-cell function did not change during the study (41.4 <plus/minus> 5.5 v 41.8 +/- 4.7, P = .478). There was no significant difference in body mass index (BMI) levels before and after the therapy (23.0 +/- 0.4 v 23.1 +/- 0.4 kg/m(2), P = .483). From these results, it can be concluded that bezafibrate reduces serum tiglycerides, insulin resistance, and fasting blood glucose levels in non-obese Japanese type 2 diabetic patients. Copyright (C) 2001 by W.B. Saunders Company.
引用
收藏
页码:477 / 480
页数:4
相关论文
共 30 条
[1]   TOWARD PHYSIOLOGICAL UNDERSTANDING OF GLUCOSE-TOLERANCE - MINIMAL-MODEL APPROACH [J].
BERGMAN, RN .
DIABETES, 1989, 38 (12) :1512-1527
[2]   DIMINISHED INSULIN-RECEPTORS ON MONOCYTES AND ERYTHROCYTES IN HYPERTRIGLYCERIDEMIA [J].
BIEGER, WP ;
MICHEL, G ;
BARWICH, D ;
BIEHL, K ;
WIRTH, A .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1984, 33 (11) :982-987
[3]   Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity - Studies in subjects with various degrees of glucose tolerance and insulin sensitivity [J].
Bonora, E ;
Saggiani, F ;
Targher, G ;
Zenere, MB ;
Alberiche, M ;
Monauni, T ;
Bonadonna, RC ;
Muggeo, M .
DIABETES CARE, 2000, 23 (01) :57-63
[4]   DO BLACKS WITH NIDDM HAVE AN INSULIN-RESISTANCE SYNDROME [J].
CHAIKEN, RL ;
BANERJI, MA ;
HUEY, H ;
LEBOVITZ, HE .
DIABETES, 1993, 42 (03) :444-449
[5]   THE TRIUMVIRATE - BETA-CELL, MUSCLE, LIVER - A COLLUSION RESPONSIBLE FOR NIDDM [J].
DEFRONZO, RA .
DIABETES, 1988, 37 (06) :667-687
[6]   Homeostasis model assessment as a clinical index of insulin resistance in type 2 diabetic patients treated with sulfonylureas [J].
Emoto, M ;
Nishizawa, Y ;
Maekawa, K ;
Hiura, Y ;
Kanda, H ;
Kawagishi, T ;
Shoji, T ;
Okuno, Y ;
Morii, H .
DIABETES CARE, 1999, 22 (05) :818-822
[7]   Homeostasis model assessment as a clinical index of insulin resistance - Comparison with the minimal model analysis [J].
Fukushima, M ;
Taniguchi, A ;
Sakai, M ;
Doi, K ;
Nagasaka, S ;
Tanaka, H ;
Tokuyama, K ;
Nakai, Y .
DIABETES CARE, 1999, 22 (11) :1911-1912
[8]   The genetic basis of type 2 diabetes mellitus: Impaired insulin secretion versus impaired insulin sensitivity [J].
Gerich, JE .
ENDOCRINE REVIEWS, 1998, 19 (04) :491-503
[9]   Insulin sensitivity in subjects with type 2 diabetes - Relationship to cardiovascular risk factors: the Insulin Resistance Atherosclerosis Study [J].
Haffner, SM ;
D'Agostino, R ;
Mykkanen, L ;
Tracy, R ;
Howard, B ;
Rewers, M ;
Selby, J ;
Savage, PJ ;
Saad, MF .
DIABETES CARE, 1999, 22 (04) :562-568
[10]   Comparison of insulin sensitivity tests across a range of glucose tolerance from normal to diabetes [J].
Hermans, MP ;
Levy, JC ;
Morris, RJ ;
Turner, RC .
DIABETOLOGIA, 1999, 42 (06) :678-687