PMID- 23269411
OWN - NLM
STAT- MEDLINE
DCOM- 20130416
LR  - 20220410
IS  - 1522-1555 (Electronic)
IS  - 0193-1849 (Print)
IS  - 0193-1849 (Linking)
VI  - 304
IP  - 5
DP  - 2013 Mar 1
TI  - Inflammation during obesity is not all bad: evidence from animal and human 
      studies.
PG  - E466-77
LID - 10.1152/ajpendo.00266.2012 [doi]
AB  - Chronic inflammation is a characteristic of obesity and is associated with 
      accompanying insulin resistance, a hallmark of type 2 diabetes mellitus (T2DM). 
      Although proinflammatory cytokines are known for their detrimental effects on 
      adipose tissue function and insulin sensitivity, their beneficial effects in the 
      regulation of metabolism have not drawn sufficient attention. In obesity, 
      inflammation is initiated by a local hypoxia to augment angiogenesis and improve 
      adipose tissue blood supply. A growing body of evidence suggests that macrophages 
      and proinflammatory cytokines are essential for adipose remodeling and adipocyte 
      differentiation. Phenotypes of multiple lines of transgenic mice consistently 
      suggest that proinflammatory cytokines increase energy expenditure and act to 
      prevent obesity. Removal of proinflammatory cytokines by gene knockout decreases 
      energy expenditure and induces adult-onset obesity. In contrast, elevation of 
      proinflammatory cytokines augments energy expenditure and decreases the risk for 
      obesity. Anti-inflammatory therapies have been tested in more than a dozen 
      clinical trials to improve insulin sensitivity and glucose homeostasis in 
      patients with T2DM, and the results are not encouraging. One possible explanation 
      is that anti-inflammatory therapies also attenuate the beneficial effects of 
      inflammation in stimulating energy expenditure, which may have limited the 
      efficacy of the treatment by promoting energy accumulation. Thus, the positive 
      effects of proinflammatory events should be considered in evaluating the impact 
      of inflammation in obesity and type 2 diabetes.
FAU - Ye, Jianping
AU  - Ye J
AD  - Antioxidant and Gene Regulation Laboratory, Pennington Biomedical Research 
      Center, Louisiana State Univ. System, Baton Rouge, LA 70808, USA. yej@pbrc.edu
FAU - McGuinness, Owen P
AU  - McGuinness OP
LA  - eng
GR  - R01 DK078188/DK/NIDDK NIH HHS/United States
GR  - DK-043748/DK/NIDDK NIH HHS/United States
GR  - DK-020593/DK/NIDDK NIH HHS/United States
GR  - R01 DK068036/DK/NIDDK NIH HHS/United States
GR  - DK-085495/DK/NIDDK NIH HHS/United States
GR  - U24 DK059637/DK/NIDDK NIH HHS/United States
GR  - DK-068036/DK/NIDDK NIH HHS/United States
GR  - P60 DK020593/DK/NIDDK NIH HHS/United States
GR  - R56 DK068036/DK/NIDDK NIH HHS/United States
GR  - R01 DK085495/DK/NIDDK NIH HHS/United States
GR  - R56 DK043748/DK/NIDDK NIH HHS/United States
GR  - DK-078188/DK/NIDDK NIH HHS/United States
GR  - DK-059637/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20121226
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Blood Glucose)
RN  - 0 (Cytokines)
RN  - 0 (Hormones)
SB  - IM
MH  - Adipose Tissue/physiopathology
MH  - Animals
MH  - Anti-Inflammatory Agents/therapeutic use
MH  - Blood Glucose/metabolism
MH  - Cytokines/metabolism
MH  - Diabetes Mellitus, Type 2/physiopathology
MH  - Energy Metabolism/physiology
MH  - Homeostasis/physiology
MH  - Hormones/metabolism
MH  - Humans
MH  - Inflammation/complications/drug therapy/*physiopathology
MH  - Insulin Resistance
MH  - Obesity/complications/*physiopathology
PMC - PMC3774179
EDAT- 2012/12/28 06:00
MHDA- 2013/04/17 06:00
PMCR- 2014/03/01
CRDT- 2012/12/28 06:00
PHST- 2012/12/28 06:00 [entrez]
PHST- 2012/12/28 06:00 [pubmed]
PHST- 2013/04/17 06:00 [medline]
PHST- 2014/03/01 00:00 [pmc-release]
AID - ajpendo.00266.2012 [pii]
AID - E-00266-2012 [pii]
AID - 10.1152/ajpendo.00266.2012 [doi]
PST - ppublish
SO  - Am J Physiol Endocrinol Metab. 2013 Mar 1;304(5):E466-77. doi: 
      10.1152/ajpendo.00266.2012. Epub 2012 Dec 26.