Home >> Annals of the New York Academy of Sciences, Volume 1084, Number 1

Inflammation in Metabolic Syndrome and Type 2 Diabetes: Impact of Dietary Glucose

Authors: KEMPF, KERSTIN; ROSE, BETTINA; HERDER, CHRISTIAN; KLEOPHAS, URSULA; MARTIN, STEPHAN; KOLB, HUBERT

Source: Annals of the New York Academy of Sciences, Volume 1084, Number 1, November 2006 , pp. 30-48(19)

Publisher: Wiley-Blackwell

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Abstract:

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Chronic overnutrition combined with a lack of exercise is the main cause for the rapidly increasing prevalence of overweight and obesity. It seems accepted that adipositis (macrophage infiltration and inflammation of adipose tissue in obesity) and systemic low grade inflammation affect the pathogenesis of the metabolic syndrome or type 2 diabetes mellitus (T2DM). Therefore, modern weight reduction programs additionally focus on strategies to attenuate the inflammation state. Exercise is one major factor, which contributes to the reduction of both the incidence of T2DM and inflammation, and the immunomodulatory effects of exercise are supported by similarly beneficial effects of dietary changes. In this context, glucose is the most extensively studied nutrient and current investigations focus on postprandial glucose-induced inflammation, one possible reason why hyperglycemia is detrimental. Indeed, glucose may modulate the mRNA expression and serum concentrations of immune parameters but these alterations rapidly normalize in normoglycemic subjects. In case of an impaired metabolic state, however, postprandial hyperglycemia increases magnitude and duration of systemic inflammatory responses, which probably promotes the development of T2DM and of cardiovascular disease.

Keywords: type 2 diabetes; obesity; inflammation; lifestyle; exercise; nutrition; glucose

Document Type: Research article

DOI: http://dx.doi.org/10.1196/annals.1372.012

Affiliations: 1: German Diabetes Clinic, German Diabetes Center, Leibniz Institute at Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany

Publication date: 2006-11-01

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