Pathophysiology and prevention of type 2 diabetes

被引:1
作者
Martin, Stephan [1 ]
Kempf, Kerstin [1 ]
Roehling, Martin [1 ]
机构
[1] Westdeutsch Diabet & Gesundheitszentrum WDGZ, VKKD, Hohensandweg 37, D-40591 Dusseldorf, Germany
来源
DIABETOLOGE | 2019年 / 15卷 / 05期
关键词
Hyperinsulinemia; Low-carbohydrate diet; Insulin; Diet; formula diet; Life style; INSULIN SENSITIVITY; HYPERINSULINEMIA; SECRETION; GLUCOSE; CARBOHYDRATE; CLEARANCE; FRUCTOSE; OBESITY; GOT;
D O I
10.1007/s11428-019-0483-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
This review article summarizes new findings from pathophysiology and prevention of type2 diabetes that have been previously presented in the Diabetes Update during the past two years. Increasing evidence suggests that exogenous and endogenous factors induce hyperinsulinemia which leads not only to insulin resistance but also causally to obesity, which is in turn induced by an unfavorable lifestyle. Moreover, it has been shown that carbohydrate-rich or hypercaloric food reduces the insulin clearance in the liver. Furthermore, anti-incretins were also discussed as inducing food-related insulin resistance. Mutations of SGLT-1 receptors (SGLT: sodium dependent glucose transporter) that lead to adecreased glucose intake are associated with areduced prevalence of obesity, diabetes mellitus and heart failure along with areduced mortality rate. During the past few years diabetes research has primarily focused on primary prevention of type2 diabetes; however, several studies for secondary prevention using non-pharmacological treatments have been published and show promising results. The DiRECT (Diabetes REmission Clinical Trial) study showed for the first time that arigorous weight reduction program using formula diets can induce clinical remissions of type2 diabetes. As aresult, formula diets as therapy options for lifestyle interventions were incorporated in the consensus report of the American Diabetes Association (ADA) and European Association for the Study of Diabetes (EASD).
引用
收藏
页码:382 / 391
页数:10
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