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Type 2 diabetes (T2D) has been associated with hepatitis C virus (HCV) infection as an independent risk factor. The increased insulin resistance induced by the HCV core protein or the treatment with interferon-based therapy (IBT) may have a role (1). It is generally agreed that IBT for patients with chronic hepatitis C (CHC) may trigger short-term insulin resistance. However, the long-term risk of developing T2D for CHC patients with IBT remains unclear. Studies suggested that if viral clearance is achieved after IBT, the risk of T2D might be reduced by two-thirds in CHC patients (2,3). An Italian study argued that a lower insulin resistance at baseline may be the reason for reduced risk of T2D (4). We therefore conducted a retrospective cohort study, using insurance claims data of Taiwan, to examine 1 ) whether CHC patients are at an elevated risk of developing T2D and 2 ) whether CHC patients receiving IBT are at a reduced risk of T2D, not only through viral clearance but also through possible alterations of glucose metabolism. The health insurance of Taiwan is a universal insurance system with 99% of all 23 million residents covered. We used a subset of claims data of 1 million beneficiaries randomly selected from all residents to …

OBJECTIVE—To study the effect of body composition and adiponectin on insulin resistance and β-cell function in schoolchildren during puberty. RESEARCH DESIGN AND METHODS—Plasma adiponectin level and its relationships with insulin sensitivity and β-cell function were analyzed in 500 randomly recruited nondiabetic Taiwanese schoolchildren (245 boys and 255 girls) aged 6–18 years in a national survey program for diabetes in 1999. Insulin resistance and β-cell function were evaluated by homeostasis model assessment (HOMA). Plasma adiponectin concentrations were determined with radioimmunoassay. RESULTS—Plasma glucose levels remained stable, whereas insulin resistance increased with a compensatory rise in β-cell function during this period. A transient drop of adiponectin level with a trough at 10–12 years was found in boys but not in girls. This pubertal drop of adiponectin levels in boys coincides with the sharp rise in testosterone concentration. A negative correlation between testosterone levels and adiponectin concentration was also noted in boys (r = −0.142, P = 0.032). Plasma adiponectin levels correlated inversely with relative body weight, fasting insulin concentrations, and insulin resistance index by HOMA in boys aged 15–18 years and in girls aged 11–14 years. No association was observed between adiponectin levels and β-cell function by HOMA. CONCLUSIONS—There is a transient drop in the level of adiponectin during male puberty, correlated with the increase in testosterone level in boys. Plasma adiponectin levels were inversely correlated with obesity and insulin resistance in boys and girls during the pubertal period.

OBJECTIVE—To study the effect of birth weight on risk of type 2 diabetes in the schoolchildren in Taiwan. RESEARCH DESIGN AND METHODS—From 1992 to 1997, all schoolchildren aged 6–18 years were screened for diabetes in Taiwan Province. This cohort consisted of 1,966 patients with diabetes and 1,780 randomly selected subjects with normal fasting glycemia (NFG). Questionnaire interviewing was designed to classify diabetes. The birth weight was obtained from the Taiwan’s Birth Registry. After merging the data, there were 978 subjects, including 429 with type 2 diabetes and 549 with of NFG enrolled in the present analyses. RESULTS—The odds ratios (95% CI) for type 2 diabetes, after adjusting age, sex, BMI, family history of diabetes, and socioeconomic status, were 2.91 (1.25–6.76) for children with low birth weight ( CONCLUSIONS—A U-shaped relationship between birth weight and risk of type 2 diabetes was found in the schoolchildren aged 6–18 years in Taiwan. Schoolchildren with type 2 diabetes who were born with low birth weight had different metabolic phenotypes compared with those born with high birth weight.

Diabetes is associated with an increased risk of various forms of cancer, such as cancer of the liver, colon, pancreas, breast, bladder, and kidney. Metformin, widely given to patients with type 2 diabetes, works by inhibiting hepatic glucose production through an LKB1 (serine-threonine liver kinase B1)/AMP-activated protein kinase (AMPK)–mediated mechanism. LKB1 is a well-recognized tumor suppressor. Activation of AMPK by LKB1 plays an important role in inhibiting cell growth. It has been suggested that metformin use in patients with diabetes may reduce their risk of cancer (1). Some studies have reported that diabetic patients taking metformin showed decreased cancer risk (2,3). However, several studies have shown that metformin does not reduce the risk of cancer in patients with diabetes (4,5). Little information is available on the subject considering non-Caucasian ethnicity. We used representative National Health Insurance datasets for Taiwan to form a cohort to …

We read with interest the article by Eppens et al. (1) concerning the prevalence of diabetes complications in adolescents with type 2 compared with type 1 diabetes. Because the study was clinic based and included a relatively small number of subjects with type 2 diabetes ( n = 68), we present our findings from a nationwide screening program, which was conducted between 1992 and 1997 for all schoolchildren aged 6–18 years (2). Diabetes was diagnosed in 381 boys and 454 girls …