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作者：Laurie Barclay, MD  
出處：WebMD醫學新聞

　　May 28, 2010 — 根據線上發表於5月18日糖尿病照護(Diabetes Care)期刊的研究結果，腰圍和體重增加可以預測偶發性糖尿病。
　　
　　法國de Rennes大學醫學中心的Alain Gautier醫師以及「Data from an Epidemiological Study on the Insulin Resistance syndrome (D.E.S.I.R.)」研究小組的夥伴寫道，空腹血糖不佳(impaired fasting glucose，IFG)者發生第2型糖尿病的風險較高，雖然內臟脂肪和腰圍是第2型糖尿病最強的風險因素，但是未曾對那些在開始時為IFG者其腰圍增加的後果進行充分研究，特別是那些在開始時未過重或肥胖者。這篇報告探討那些開始時為IFG者，腰圍和體重增加對於發生糖尿病的相對重要性，根據開始時的BMI分組。
　　
　　研究者針對D.E.S.I.R.世代探討979名開始時為IFG之男性和女性的9年糖尿病發生率，校正開始時的風險因素之後，腰圍和體重增加都和糖尿病發生率有顯著相關。腰圍的標準勝算比(ORs)是1.79 (95%信心區間[CI]為1.45 - 2.21)，體重則是1.86(95% CI，1.51 - 2.30)。
　　
　　相較於開始時BMI大於等於25 kg/m2的病患(OR為1.66；95% CI為1.28 - 2.16)，開始時BMI小於25 kg/m2的病患，腰圍增加的影響較大(OR為2.40；95% CI，1.63 - 3.52)。校正同時發生的胰島素血症或更新版胰島素抗性指標(HOMA2-IR)改變，並未消除BMI變化的影響差異，兩個BMI組的體重改變效果相似。
　　
　　研究作者寫道，在IFG者，重點在監測與預防腰圍增加，特別是那些BMI小於25 kg/m2者。
　　
　　研究限制包括，缺乏胰島素敏感性的黃金標準測量，例如血糖鉗定術( euglycemic-hyperinsulinemic clamp)。
　　
　　研究作者寫道，不佳的β-細胞功能被視為IFG者的一個重要特徵，胰島素分泌減少顯示一個導致體型瘦者發生糖尿病的重要機轉，我們推測，腰圍增加可能會減少胰島素分泌的後續變化，此外也包括胰島素阻抗性惡化。可能的機轉包括β-細胞的脂毒性：促進脂肪組織釋出游離的脂肪酸。
　　
　　D.E.S.I.R.研究接受INSERM和CNAMTS、Lilly、Novartis Pharma與Sanofi-Aventis的合約支持；以及INSERM (Reseaux en Sante Publique、Interactions entre les determinants de la sante、Cohortes Sante TGIR 2008)、Diabete Risque Vasculaire協會、Federation Francaise de Cardiologie、La Fondation de France、ALFEDIAM、 ONIVINS、Ardix Medical、Bayer Diagnostics、Becton Dickinson、Cardionics、Merck Sante、Novo Nordisk、 Pierre Fabre、Roche與Topcon的支持。研究作者們皆宣告沒有相關財務關係。
　　
　　Diabetes Care. 線上發表於2010年5月18日。


Increases in Waist Circumference and Weight May Predict Incident Diabetes

By Laurie Barclay, MD
Medscape Medical News

May 28, 2010 — Increases in waist circumference and weight may predict incident diabetes, according to the results of a study reported online May 18 in Diabetes Care.

"Individuals with impaired fasting glucose (IFG) are at high risk for type 2 diabetes," write Alain Gautier, MD, from Center Hospitalier Universitaire de Rennes in France, and colleagues from the Data from an Epidemiological Study on the Insulin Resistance syndrome (D.E.S.I.R.) Study Group. "Although visceral adiposity and waist circumference are strong risk factors for type 2 diabetes, the consequence of an increase in waist circumference among individuals with IFG at baseline has not been fully investigated, in particular in those who are not overweight or obese at baseline. This report investigates the relative importance of increases in waist circumference and weight on progression to diabetes, in individuals with baseline IFG, according to baseline BMI [body mass index] strata."

Using the D.E.S.I.R. cohort, the investigators studied the 9-year incidence of diabetes in 979 men and women with baseline IFG. After adjustment for risk factors at baseline, increases in both waist circumference and weight were significantly associated with diabetes incidence. Standardized odds ratios (ORs) were 1.79 for waist circumference (95% confidence interval [CI], 1.45 - 2.21) and 1.86 for weight (95% CI, 1.51 - 2.30).

For patients with a BMI of less than 25 kg/m2 at baseline, the effect of increase in waist circumference was greater (OR, 2.40; 95% CI, 1.63 - 3.52) vs patients with a BMI of 25 kg/m2 or more at baseline (OR, 1.66; 95% CI, 1.28 - 2.16). Adjustment for concurrent changes in either insulinemia or the updated version of the homeostasis model assessment of insulin resistance (HOMA2-IR) index did not abolish the difference in effect based on initial BMI. The effect of weight change was similar in both BMI groups.

"In IFG individuals, it is important to monitor and prevent increases in waist circumference, in particular for those with BMI<25 kg/m2," the study authors write.

Limitations of this study include absence of gold-standard measures of insulin sensitivity, such as the euglycemic-hyperinsulinemic clamp.

"Impaired β-cell function is considered an important characteristic in individuals with IFG and reduced insulin secretion has been shown to be a prominent mechanism leading to diabetes in lean individuals," the study authors write. "We speculate that an increase in waist circumference may induce further alterations in insulin secretion beyond that inherent in a worsening insulin resistance. Potential mechanisms may involve β-cell lipotoxicity through enhanced free fatty acid release from adipose tissue."

The D.E.S.I.R. study has been supported by INSERM contracts with CNAMTS, Lilly, Novartis Pharma, and Sanofi-Aventis; by INSERM (Reseaux en Sante Publique, Interactions entre les determinants de la sante, Cohortes Sante TGIR 2008), the Association Diabete Risque Vasculaire, the Federation Francaise de Cardiologie, La Fondation de France, ALFEDIAM, ONIVINS, Ardix Medical, Bayer Diagnostics, Becton Dickinson, Cardionics, Merck Sante, Novo Nordisk, Pierre Fabre, Roche, and Topcon. The study authors have disclosed no relevant financial relationships.

Diabetes Care. Published online May 18, 2010.