title: Inflammation in metabolic syndrome and type 2 diabetes: Impact of dietary glucose.
abstract: 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.
authors.affiliation: German Diabetes Clinic, German Diabetes Center, Leibniz Institute at Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany. kerstin.kempf@ddz.uni-duesseldorf.de
authors.forename: Kerstin
authors.initials: K
authors.lastname: Kempf
authors.forename: Bettina
authors.initials: B
authors.lastname: Rose
authors.forename: Christian
authors.initials: C
authors.lastname: Herder
authors.forename: Ursula
authors.initials: U
authors.lastname: Kleophas
authors.forename: Stephan
authors.initials: S
authors.lastname: Martin
authors.forename: Hubert
authors.initials: H
authors.lastname: Kolb
mesh_terms: D016207:Cytokines / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D004040:Dietary Carbohydrates; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D024821:Metabolic Syndrome / Q000503:physiopathology*; D012333:RNA, Messenger / Q000235:genetics; D014158:Transcription, Genetic / Q000187:drug effects
chemical_list: D016207:Cytokines; D004040:Dietary Carbohydrates; D007328:Insulin; D012333:RNA, Messenger; D005947:Glucose