PMID- 29713651
OWN - NLM
STAT- MEDLINE
DCOM- 20181002
LR  - 20220317
IS  - 2314-6753 (Electronic)
IS  - 2314-6745 (Print)
VI  - 2018
DP  - 2018
TI  - Novel Mechanisms Modulating Palmitate-Induced Inflammatory Factors in 
      Hypertrophied 3T3-L1 Adipocytes by AMPK.
PG  - 9256482
LID - 10.1155/2018/9256482 [doi]
LID - 9256482
AB  - OBJECTIVE: A growing body of evidence indicates that AMP-activated protein kinase 
      (AMPK) contributes to not only energy metabolic homeostasis but also the 
      inhibition of inflammatory responses. However, the underlying mechanisms remain 
      unclear. To elucidate the role of AMPK, in this study, we observed the effects of 
      AMPK activation on monocyte chemoattractant protein-1 (MCP-1) release in mature 
      3T3-L1 adipocytes. METHODS: We observed signal transduction pathways regulating 
      MCP-1, which increased in obese adipocytes, in an in vitro model of hypertrophied 
      3T3-L1 adipocytes preloaded with palmitate. RESULTS: Palmitate-preloaded cells 
      exhibited significant increase in MCP-1 release and triglyceride (TG) deposition. 
      Increased MCP-1 release and TG deposition were significantly decreased by an AMPK 
      activator. In addition, the AMPK activator not only markedly diminished MCP-1 
      secretion but also augmented phosphorylation of nuclear factor-kappaB (NF-kappaB) and 
      extracellular signal-regulated kinase (ERK) 1/2. In contrast, MCP-1 release 
      suppression was abolished by the AMPK inhibitor compound C and the MEK inhibitor 
      U0126. CONCLUSIONS: MCP-1 release from hypertrophied adipocytes is suppressed by 
      AMPK activation through the NF-kappaB and ERK pathways. These findings provide 
      evidence that AMPK plays a crucial role in ameliorating obesity-induced 
      inflammation.
FAU - Morita, Naru
AU  - Morita N
AUID- ORCID: 0000-0003-2942-8441
AD  - Third Department of Internal Medicine, Division of Diabetes, Endocrinology and 
      Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
FAU - Hosaka, Toshio
AU  - Hosaka T
AD  - Third Department of Internal Medicine, Division of Diabetes, Endocrinology and 
      Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
FAU - Kitahara, Atsuko
AU  - Kitahara A
AD  - Third Department of Internal Medicine, Division of Diabetes, Endocrinology and 
      Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
FAU - Murashima, Toshitaka
AU  - Murashima T
AD  - Third Department of Internal Medicine, Division of Diabetes, Endocrinology and 
      Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
FAU - Onuma, Hirohisa
AU  - Onuma H
AD  - Third Department of Internal Medicine, Division of Diabetes, Endocrinology and 
      Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
FAU - Sumitani, Yoshikazu
AU  - Sumitani Y
AD  - Third Department of Internal Medicine, Division of Diabetes, Endocrinology and 
      Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
FAU - Takahashi, Kazuto
AU  - Takahashi K
AUID- ORCID: 0000-0002-6887-1481
AD  - Third Department of Internal Medicine, Division of Diabetes, Endocrinology and 
      Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
FAU - Tanaka, Toshiaki
AU  - Tanaka T
AD  - Third Department of Internal Medicine, Division of Diabetes, Endocrinology and 
      Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
FAU - Kondo, Takuma
AU  - Kondo T
AD  - Third Department of Internal Medicine, Division of Diabetes, Endocrinology and 
      Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
FAU - Ishida, Hitoshi
AU  - Ishida H
AUID- ORCID: 0000-0001-6603-6709
AD  - Third Department of Internal Medicine, Division of Diabetes, Endocrinology and 
      Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
LA  - eng
PT  - Journal Article
DEP - 20180311
PL  - England
TA  - J Diabetes Res
JT  - Journal of diabetes research
JID - 101605237
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (Ribonucleotides)
RN  - 0 (Triglycerides)
RN  - 2V16EO95H1 (Palmitic Acid)
RN  - 360-97-4 (Aminoimidazole Carboxamide)
RN  - 9100L32L2N (Metformin)
RN  - EC 2.7.4.3 (Adenylate Kinase)
RN  - F0X88YW0YK (AICA ribonucleotide)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adenylate Kinase/*metabolism
MH  - Adipocytes/drug effects/*metabolism
MH  - Aminoimidazole Carboxamide/analogs & derivatives/pharmacology
MH  - Animals
MH  - Chemokine CCL2/*metabolism
MH  - Inflammation/*metabolism
MH  - Metformin/pharmacology
MH  - Mice
MH  - NF-kappa B/metabolism
MH  - Palmitic Acid/*pharmacology
MH  - Phosphorylation/drug effects
MH  - Ribonucleotides/pharmacology
MH  - Signal Transduction/*drug effects
MH  - Triglycerides/metabolism
PMC - PMC5866861
EDAT- 2018/05/02 06:00
MHDA- 2018/10/03 06:00
PMCR- 2018/03/11
CRDT- 2018/05/02 06:00
PHST- 2017/10/24 00:00 [received]
PHST- 2018/01/10 00:00 [revised]
PHST- 2018/01/21 00:00 [accepted]
PHST- 2018/05/02 06:00 [entrez]
PHST- 2018/05/02 06:00 [pubmed]
PHST- 2018/10/03 06:00 [medline]
PHST- 2018/03/11 00:00 [pmc-release]
AID - 10.1155/2018/9256482 [doi]
PST - epublish
SO  - J Diabetes Res. 2018 Mar 11;2018:9256482. doi: 10.1155/2018/9256482. eCollection 
      2018.