PMID- 23431246
OWN - NLM
STAT- MEDLINE
DCOM- 20130819
LR  - 20211021
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2013
DP  - 2013
TI  - An anti-inflammatory sterol decreases obesity-related inflammation-induced 
      insulin resistance and metabolic dysregulation.
PG  - 814989
LID - 10.1155/2013/814989 [doi]
LID - 814989
AB  - Obesity-related inflammation-induced insulin resistance and metabolic 
      dysregulation were investigated in retrospective analysis of placebo hematologic 
      and metabolic laboratory data from trials associated with increasing chronic 
      low-grade inflammation and body mass index. Studies included healthy subjects and 
      those with progressive stages of metabolic dysregulation, including type 2 
      diabetes mellitus with uncontrolled hemoglobin A1c. Intrasubject variances in 
      erythroid and metabolic values increased with metabolic dysregulation. Random 
      effects were demonstrated in treatment-naive diabetes for erythroid, glucose, and 
      HbA1c fluctuations. The anti-inflammatory insulin sensitizer, HE3286, was tested 
      for its ability to decrease obesity-related inflammation-induced insulin 
      resistance and metabolic dysregulation in diabetes. HE3286 significantly 
      decreased erythroid and metabolic variances and improved 1,5-anhydroglucitol (a 
      surrogate of postprandial glucose) compared to the placebo group. HE3286 HbA1c 
      decrease correlated with weight loss and inversely with baseline monocyte 
      chemoattractant protein-1 (MCP-1) in metformin-treated diabetics. Normalization 
      of HbA1c to the 84-day average hemoglobin revealed that HE3286 HbA1c decrease 
      correlated with high baseline MCP-1 and MCP-1 decrease in treatment-naive 
      diabetics. HE3286 decreased insulin resistance, increased the frequency of 
      decreased day 84 HbA1c in metformin-treated subjects, and decreased day 112 HbA1c 
      in treatment-naive diabetics. HE3286 may be useful to restore metabolic 
      homeostasis in type 2 diabetes.
FAU - Reading, Chris L
AU  - Reading CL
AD  - Harbor Therapeutics, Inc., San Diego, CA 92122, USA. creading@harbortx.com
FAU - Flores-Riveros, Jaime
AU  - Flores-Riveros J
FAU - Stickney, Dwight R
AU  - Stickney DR
FAU - Frincke, James M
AU  - Frincke JM
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
DEP - 20130130
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Sterols)
SB  - IM
MH  - Adult
MH  - Anti-Inflammatory Agents/*therapeutic use
MH  - Female
MH  - Humans
MH  - Inflammation/*complications
MH  - Insulin Resistance/*physiology
MH  - Male
MH  - Middle Aged
MH  - Obesity/*drug therapy/*immunology
MH  - Sterols/*therapeutic use
PMC - PMC3572652
EDAT- 2013/02/23 06:00
MHDA- 2013/08/21 06:00
PMCR- 2013/01/30
CRDT- 2013/02/23 06:00
PHST- 2012/11/16 00:00 [received]
PHST- 2012/12/18 00:00 [revised]
PHST- 2012/12/20 00:00 [accepted]
PHST- 2013/02/23 06:00 [entrez]
PHST- 2013/02/23 06:00 [pubmed]
PHST- 2013/08/21 06:00 [medline]
PHST- 2013/01/30 00:00 [pmc-release]
AID - 10.1155/2013/814989 [doi]
PST - ppublish
SO  - Mediators Inflamm. 2013;2013:814989. doi: 10.1155/2013/814989. Epub 2013 Jan 30.