PMID- 22683098
OWN - NLM
STAT- MEDLINE
DCOM- 20121228
LR  - 20181202
IS  - 1532-8600 (Electronic)
IS  - 0026-0495 (Linking)
VI  - 61
IP  - 11
DP  - 2012 Nov
TI  - Differential nitric oxide levels in the blood and skeletal muscle of type 2 
      diabetic subjects may be consequence of adiposity: a preliminary study.
PG  - 1528-37
LID - S0026-0495(12)00177-1 [pii]
LID - 10.1016/j.metabol.2012.05.003 [doi]
AB  - BACKGROUND AND AIMS: Nitric oxide (NO.) exerts key regulatory functions including 
      vasodilation and glucose uptake. Thus reduced NO. levels are associated with 
      insulin resistance and hypertension. In this preliminary work we aimed to measure 
      the levels of NO. metabolites in serum and skeletal muscle of obese and non-obese 
      subjects, with or without type 2 diabetes mellitus (T2DM). METHODS: Fifteen 
      sedentary male participants [7 obese controls (C) vs 5 obese and 3 non-obese 
      T2DM; age 54+/-9 years] were selected according to their BMI (>30 kg/m(2) for obese 
      and 23-27 kg/m(2) for non-obese participants) and evaluated for fasted values of 
      blood glucose, HbA1c, lipid profile, serum CRP (C-reactive protein), erythrocyte 
      glutathione (GSH) metabolism, plasma adiponectin, leptin and cytokines (TNF-alpha and 
      INFgamma), serum and skeletal muscle nitric oxide metabolites (nitrite and nitrates; 
      tNOx) and skeletal muscle nNOS and iNOS expression. Body composition was measured 
      by whole body DEXA and muscle microbiopsy was performed in the vastus lateralis. 
      RESULTS: We found that serum tNOx (total nitrite/nitrate; mumol/L) was lower in 
      obese T2DM group (12.7+/-3.5) when compared with their controls (21.1+/-2.4), 
      although the non-obese group presented higher concentration of tNOx (33.8+/-7.2). 
      Skeletal muscle nNOS was higher in obese controls, lower in non-obese T2DM and 
      undetected in obese T2DM. On the other hand, expression of iNOS had an inverse 
      relationship with nNOS, showing higher expression in obese T2DM, decrease in 
      non-obese T2DM and absence in obese control group. tNOx levels (mumol/mg protein) 
      were decreased in the non-obese T2DM group (12.07+/-0.59) when compared with the 
      obese control (21.68+/-6.2) and the obese T2DM group (26.3+/-7.26). CONCLUSION: We 
      conclude that the decreased serum NO∙ production in obese T2DM patients seems to 
      be associated with adipose mass as lower adiposity was associated with normal NO∙ 
      which was reduced in the skeletal muscle of the non-obese T2DM patients. We 
      suggest that the lower adiposity (and higher adiponectin) in non-obese T2DM could 
      be responsible for differential levels of NO∙ production and insulin resistance.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Krause, Mauricio
AU  - Krause M
AD  - Biomedical Research Group, Department of Science, Institute of Technology 
      Tallaght Dublin, Ireland. mauriciokrause@hotmail.com
FAU - Rodrigues-Krause, Josianne
AU  - Rodrigues-Krause J
FAU - O'Hagan, Ciara
AU  - O'Hagan C
FAU - De Vito, Giuseppe
AU  - De Vito G
FAU - Boreham, Colin
AU  - Boreham C
FAU - Susta, Davide
AU  - Susta D
FAU - Newsholme, Philip
AU  - Newsholme P
FAU - Murphy, Colin
AU  - Murphy C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120607
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type I)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
SB  - IM
MH  - *Adiposity
MH  - Body Mass Index
MH  - Case-Control Studies
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Muscle, Skeletal/enzymology/*metabolism
MH  - Nitric Oxide/*blood/metabolism
MH  - Nitric Oxide Synthase Type I/metabolism
MH  - Nitric Oxide Synthase Type II/metabolism
MH  - Obesity/blood/metabolism
MH  - Sedentary Behavior
EDAT- 2012/06/12 06:00
MHDA- 2012/12/29 06:00
CRDT- 2012/06/12 06:00
PHST- 2012/03/05 00:00 [received]
PHST- 2012/04/24 00:00 [revised]
PHST- 2012/05/02 00:00 [accepted]
PHST- 2012/06/12 06:00 [entrez]
PHST- 2012/06/12 06:00 [pubmed]
PHST- 2012/12/29 06:00 [medline]
AID - S0026-0495(12)00177-1 [pii]
AID - 10.1016/j.metabol.2012.05.003 [doi]
PST - ppublish
SO  - Metabolism. 2012 Nov;61(11):1528-37. doi: 10.1016/j.metabol.2012.05.003. Epub 
      2012 Jun 7.