title: A low-glycemic index diet and exercise intervention reduces TNF(alpha) in isolated mononuclear cells of older, obese adults.
abstract: Low-glycemic index diets and exercise independently improve glucose tolerance and reduce diabetes risk. However, the combined effect of a low-glycemic index diet and exercise on inflammation and glucose metabolism is not known. Therefore, we randomized 28 insulin-resistant adults (age: 66 ± 1 y; BMI: 34.2 ± 0.7 kg · m(-2)) to a 12-wk, low (LGI = 40) or high- (HGI = 80) glycemic index diet plus aerobic exercise (5 d · wk(-1), 60 min · d(-1), 80-85% heart rate(max)) intervention. All food and fluids were provided during the study. Inflammation was assessed from cytokine (TNFα and IL-6) secretion using peripheral blood mononuclear cells (MNC) stimulated overnight with LPS. Glycemic response was determined following ingestion of a 75-g glucose solution. Fasting blood samples were collected for additional cytokine [TNFα, IL-6, and monocyte chemoattractant protein 1 (MCP-1)] analysis. Both interventions decreased BMI (P < 0.001), fasting plasma glucose (P = 0.01), and insulin (P = 0.02). The glycemic response was reduced only in the LGI group (P = 0.04). Plasma and MNC-derived TNFα secretion were reduced in the LGI group (P = 0.02) but increased in the HGI group (P = 0.02). Secretion of IL-6 from MNC and plasma IL-6 and MCP-1 concentrations were reduced in the LGI group. The change in MNC-derived TNFα (r = 0.43; P = 0.04) and plasma MCP-1 (r = 0.44; P = 0.04) correlated with decreases in the glycemic response. These data highlight the importance of diet composition in the treatment and prevention of inflammation and hyperglycemia. A low-glycemic index diet has antiinflammatory and antidiabetogenic effects when combined with exercise in older, obese prediabetics.
authors.affiliation: Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA. karen.kelly@med.navy.mil
authors.forename: Karen R
authors.initials: KR
authors.lastname: Kelly
authors.forename: Jacob M
authors.initials: JM
authors.lastname: Haus
authors.forename: Thomas P J
authors.initials: TP
authors.lastname: Solomon
authors.forename: Aimee J
authors.initials: AJ
authors.lastname: Patrick-Melin
authors.forename: Marc
authors.initials: M
authors.lastname: Cook
authors.forename: Michael
authors.initials: M
authors.lastname: Rocco
authors.forename: Hope
authors.initials: H
authors.lastname: Barkoukis
authors.forename: John P
authors.initials: JP
authors.lastname: Kirwan
mesh_terms: D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition; D018932:Chemokine CCL2 / Q000097:blood; D003131:Combined Modality Therapy; D003924:Diabetes Mellitus, Type 2 / Q000517:prevention & control; D004032:Diet; D005081:Exercise Therapy; D005260:Female; D038321:Glycemic Index; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000097:blood; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D009765:Obesity / Q000097:blood / Q000150:complications / Q000178:diet therapy* / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D001786:Blood Glucose; C111835:CCL2 protein, human; D018932:Chemokine CCL2; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha