Document Detail


A low-glycemic index diet and exercise intervention reduces TNF(alpha) in isolated mononuclear cells of older, obese adults.
MedLine Citation:
PMID:  21525252     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Karen R Kelly; Jacob M Haus; Thomas P J Solomon; Aimee J Patrick-Melin; Marc Cook; Michael Rocco; Hope Barkoukis; John P Kirwan
Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural     Date:  2011-04-27
Journal Detail:
Title:  The Journal of nutrition     Volume:  141     ISSN:  1541-6100     ISO Abbreviation:  J. Nutr.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-23     Completed Date:  2011-08-09     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  0404243     Medline TA:  J Nutr     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1089-94     Citation Subset:  IM    
Affiliation:
Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA. karen.kelly@med.navy.mil
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MeSH Terms
Descriptor/Qualifier:
Aged
Blood Glucose / metabolism
Body Composition
Chemokine CCL2 / blood
Combined Modality Therapy
Diabetes Mellitus, Type 2 / prevention & control
Diet*
Exercise Therapy*
Female
Glycemic Index
Humans
Inflammation Mediators / blood
Insulin Resistance
Interleukin-6 / blood
Leukocytes, Mononuclear / metabolism
Male
Obesity / blood,  complications,  diet therapy*,  therapy*
Tumor Necrosis Factor-alpha / blood*
Grant Support
ID/Acronym/Agency:
1UL1RR024989/RR/NCRR NIH HHS; R01 AG12834/AG/NIA NIH HHS; T32 DK007319/DK/NIDDK NIH HHS; T32 HL007887/HL/NHLBI NIH HHS; UL1 RR024989/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/CCL2 protein, human; 0/Chemokine CCL2; 0/IL6 protein, human; 0/Inflammation Mediators; 0/Interleukin-6; 0/Tumor Necrosis Factor-alpha
Comments/Corrections

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