PMID- 19798065
OWN - NLM
STAT- MEDLINE
DCOM- 20100902
LR  - 20220409
IS  - 1930-739X (Electronic)
IS  - 1930-7381 (Linking)
VI  - 18
IP  - 4
DP  - 2010 Apr
TI  - Dietary capsaicin reduces obesity-induced insulin resistance and hepatic 
      steatosis in obese mice fed a high-fat diet.
PG  - 780-7
LID - 10.1038/oby.2009.301 [doi]
AB  - Obesity-induced inflammation contributes to the development of obesity-related 
      metabolic disorders such as insulin resistance, type 2 diabetes, fatty liver 
      disease, and cardiovascular disease. In this study, we investigated whether 
      dietary capsaicin can reduce obesity-induced inflammation and metabolic disorders 
      such as insulin resistance and hepatic steatosis. Male C57BL/6 obese mice fed a 
      high-fat diet for 10 weeks received a supplement of 0.015% capsaicin for a 
      further 10 weeks and were compared with unsupplemented controls. Glucose 
      intolerance was estimated by glucose tolerance tests. Transcripts of 
      adipocytokine genes and the corresponding proteins were measured by reverse 
      transcription-PCR and enzyme-linked immunosorbent assay, and macrophage numbers 
      were determined by flow cytometric analysis. Transient receptor potential 
      vanilloid type-1 (TRPV-1), peroxisome proliferator-activated receptor 
      (PPAR)-alpha, and PPARgamma coactivator-1alpha (PGC-1alpha) mRNAs were also 
      measured by RT-PCR, and PPARalpha luciferase assays were performed. Dietary 
      capsaicin lowered fasting glucose, insulin, leptin levels, and markedly reduced 
      the impairment of glucose tolerance in obese mice. Levels of tumor necrosis 
      factor-alpha (TNFalpha), monocyte chemoattractant protein-1 (MCP-1), and 
      interleukin (IL)-6 mRNAs and proteins in adipose tissue and liver decreased 
      markedly, as did macrophage infiltration, hepatic triglycerides, and TRPV-1 
      expression in adipose tissue. At the same time, the mRNA/protein of adiponectin 
      in the adipose tissue and PPARalpha/PGC-1alpha mRNA in the liver increased. 
      Moreover, luciferase assays revealed that capsaicin is capable of binding 
      PPARalpha. Our data suggest that dietary capsaicin may reduce obesity-induced 
      glucose intolerance by not only suppressing inflammatory responses but also 
      enhancing fatty acid oxidation in adipose tissue and/or liver, both of which are 
      important peripheral tissues affecting insulin resistance. The effects of 
      capsaicin in adipose tissue and liver are related to its dual action on PPARalpha 
      and TRPV-1 expression/activation.
FAU - Kang, Ji-Hye
AU  - Kang JH
AD  - Department of Food Science and Nutrition, University of Ulsan, Ulsan, South 
      Korea.
FAU - Goto, Tsuyoshi
AU  - Goto T
FAU - Han, In-Seob
AU  - Han IS
FAU - Kawada, Teruo
AU  - Kawada T
FAU - Kim, Young Min
AU  - Kim YM
FAU - Yu, Rina
AU  - Yu R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20091001
PL  - United States
TA  - Obesity (Silver Spring)
JT  - Obesity (Silver Spring, Md.)
JID - 101264860
RN  - 0 (Adiponectin)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Blood Glucose)
RN  - 0 (Dietary Fats)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
RN  - 0 (Leptin)
RN  - 0 (PPAR alpha)
RN  - 0 (RNA, Messenger)
RN  - 0 (TRPV Cation Channels)
RN  - 0 (TRPV1 protein, human)
RN  - 0 (Triglycerides)
RN  - S07O44R1ZM (Capsaicin)
SB  - IM
MH  - Adiponectin/genetics/metabolism
MH  - Adipose Tissue/metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology/*therapeutic use
MH  - Blood Glucose/metabolism
MH  - Capsaicin/pharmacology/*therapeutic use
MH  - Dietary Fats/administration & dosage/metabolism
MH  - Dietary Supplements
MH  - Disease Models, Animal
MH  - Fatty Liver/*drug therapy/etiology/metabolism
MH  - Flow Cytometry
MH  - Gene Expression
MH  - Glucose Intolerance/etiology/metabolism
MH  - Hypoglycemic Agents/pharmacology/*therapeutic use
MH  - Inflammation/genetics
MH  - Insulin/blood
MH  - *Insulin Resistance
MH  - Leptin/blood
MH  - Lipid Metabolism/drug effects
MH  - Liver/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Obese
MH  - Obesity/*complications/drug therapy/metabolism
MH  - PPAR alpha/chemistry/genetics/metabolism
MH  - RNA, Messenger/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - TRPV Cation Channels/genetics/metabolism
MH  - Triglycerides/metabolism
EDAT- 2009/10/03 06:00
MHDA- 2010/09/03 06:00
CRDT- 2009/10/03 06:00
PHST- 2009/10/03 06:00 [entrez]
PHST- 2009/10/03 06:00 [pubmed]
PHST- 2010/09/03 06:00 [medline]
AID - oby2009301 [pii]
AID - 10.1038/oby.2009.301 [doi]
PST - ppublish
SO  - Obesity (Silver Spring). 2010 Apr;18(4):780-7. doi: 10.1038/oby.2009.301. Epub 
      2009 Oct 1.