PMID- 20446026
OWN - NLM
STAT- MEDLINE
DCOM- 20110616
LR  - 20211020
IS  - 1573-2576 (Electronic)
IS  - 0360-3997 (Linking)
VI  - 34
IP  - 2
DP  - 2011 Apr
TI  - High-carbohydrate diet selectively induces tumor necrosis factor-alpha production in 
      mice liver.
PG  - 139-45
LID - 10.1007/s10753-010-9217-0 [doi]
AB  - Obesity may represent a state of chronic low-grade inflammation associated with 
      infiltration of adipose tissue by inflammatory cells. Tumor necrosis factor-alpha 
      (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1/JE), two important 
      inflammatory cytokines, have been shown to be regulated according to changes in 
      body adiposity. In this study on Swiss mice, we compared the influences of 
      long-term high-carbohydrate (HC) or high-fat (HF) diet on adiposity, glucose 
      tolerance, and secretion of TNF-alpha and MCP-1/JE by adipose tissue and liver. For 
      8 weeks, male Swiss mice (7-8 weeks) were fed either standard laboratory rodent 
      diet (control group), HC diet (64% carbohydrate, 19% protein, and 11% fat), or HF 
      diet (45% carbohydrate, 17% protein, and 38% fat), with the latter two diets 
      having no fiber. Oral glucose tolerance test, triacylglycerol (TAG) plasma 
      concentration, and systemic or tissue levels of the two proinflammatory cytokines 
      were determined. Body weight increased by approximately 20% in mice fed the 
      experimental diets compared with mice fed the control diet. Systemically, the 
      hypercaloric diets induced hyperglycemia with impairment in glucose tolerance, 
      elevated circulating TAG levels, and increased plasma concentrations of TNF-alpha and 
      MCP-1/JE. In the target organs (adipose tissue and liver), both diets increased 
      MCP-1/JE levels. However, the HC diet, but not the HF diet, was able to increase 
      TNF-alpha concentration in the liver. These results have shown that the nature of 
      nutrients influences the type of proinflammatory cytokines in target organs and 
      may contribute to the comorbidities of obesity.
FAU - Ferreira, Adaliene Versiani Matos
AU  - Ferreira AV
AD  - Department of Nutrition, Nursing School, Federal University of Minas Gerais, Av. 
      Alfredo Balena 190, Belo Horizonte, MG, Brazil.
FAU - Mario, Erica Guilhen
AU  - Mario EG
FAU - Porto, Laura Cristina Jardim
AU  - Porto LC
FAU - Andrade, Silvia Passos
AU  - Andrade SP
FAU - Botion, Leida Maria
AU  - Botion LM
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Dietary Carbohydrates)
RN  - 0 (Dietary Fats)
RN  - 0 (Triglycerides)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adipose Tissue/metabolism
MH  - Adiposity
MH  - Animals
MH  - Body Weight
MH  - Chemokine CCL2/blood/*metabolism
MH  - Diet
MH  - Dietary Carbohydrates/*administration & dosage
MH  - Dietary Fats/*administration & dosage
MH  - Glucose Tolerance Test
MH  - Hyperglycemia
MH  - Liver/*metabolism
MH  - Male
MH  - Mice
MH  - Obesity/immunology/metabolism
MH  - Triglycerides/blood/metabolism
MH  - Tumor Necrosis Factor-alpha/blood/*metabolism
EDAT- 2010/05/07 06:00
MHDA- 2011/06/17 06:00
CRDT- 2010/05/07 06:00
PHST- 2010/05/07 06:00 [entrez]
PHST- 2010/05/07 06:00 [pubmed]
PHST- 2011/06/17 06:00 [medline]
AID - 10.1007/s10753-010-9217-0 [doi]
PST - ppublish
SO  - Inflammation. 2011 Apr;34(2):139-45. doi: 10.1007/s10753-010-9217-0.