scholarly journals Cannabinoid Type 1 Receptor Blockade Promotes Mitochondrial Biogenesis Through Endothelial Nitric Oxide Synthase Expression in White Adipocytes

Diabetes ◽  
2008 ◽  
Vol 57 (8) ◽  
pp. 2028-2036 ◽  
Author(s):  
L. Tedesco ◽  
A. Valerio ◽  
C. Cervino ◽  
A. Cardile ◽  
C. Pagano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mitochondrial Biogenesis ◽  
Endothelial Nitric Oxide Synthase ◽  
Receptor Blockade ◽  
Cannabinoid Type 1 Receptor ◽  
White Adipocytes ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Intron 4 a/b polymorphism of the endothelial nitric oxide synthase gene is associated with both type 1 and type 2 diabetes in a genetically homogeneous population

2008 ◽  
Vol 69 (4-5) ◽  
pp. 279-283 ◽  
Author(s):  
Emmanouil Galanakis ◽  
Diamantis Kofteridis ◽  
Kalliopi Stratigi ◽  
Eleni Petraki ◽  
Vassilios Vazgiourakis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Type 2 Diabetes ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Homogeneous Population ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Intron 4

Polymorphism in exon 7 of the endothelial nitric oxide synthase gene is associated with low incidence of microvascular damage in type 1 diabetic neuropathy

2009 ◽  
Vol 4 (4) ◽  
pp. 521-527 ◽  
Author(s):  
Constantina Heltianu ◽  
Simona-Adriana Manea ◽  
Cristian Guja ◽  
Alexandra Robciuc ◽  
Constantin Ionescu-Tirgoviste
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Diabetic Neuropathy ◽  
Endothelial Nitric Oxide Synthase ◽  
Microvascular Complications ◽  
Diabetic Patients ◽  
Enos Gene ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

AbstractMicrovascular complications associated with type 1 diabetes mellitus (T1DM) are caused in part by endothelial dysfunction. We aimed to determine the association between polymorphisms in endothelial nitric oxide synthase (eNOS) gene (894G>T, 4ab) and T1DM-associated microvascular disorders, and the roles of nitrite/nitrate products (NOx) and low molecular weight-AGEs (LMW-AGEs) levels in this relationship. We carried out a case-control study (328 subjects) and determined genotypes by PCR. The rare-type TT of eNOS 894G>T was significantly overrepresented in patients without microvascular disorders as compared with control (OR=3.64; 95% C.I.=1.02–12.73; P=0.039). The prevalence of neuropathy was high among 894GG homozygotes (OR=0.5; 95% C.I.=0.29–0.86; P=0.012) who had high levels of triglycerides, elevated systolic BP, increased NOx, and LMW-AGEs. Decreased NOx levels were associated with 894TT genotype (beta=−0.65; P=0.043) in diabetic patients prone to microvascular complications. Multiple regression analysis indicated a negative correlation between eNOS 894G>T and diabetic neuropathy (P=0.025). The distribution of eNOS 4aa genotype was high (P=0.042) in patients with T1DM; however, it does not represent a risk factor for neuropathy. The overrepresentation of eNOS 894TT genotype in diabetic patients is associated with low risk for neuropathy. Decreased NOx and LMW-AGEs levels and lower lipid profile are the main features of patients carrying the eNOS 894T allele. These data suggest that the eNOS 894TT genotype may play a protective role by preventing microvascular disorders.

scholarly journals Endothelial Nitric Oxide Synthase Knockdown in Human Stem Cells Impacts Mitochondrial Biogenesis and Adipogenesis: Live-Cell Real-Time Fluorescence Imaging

2021 ◽  
Vol 10 (4) ◽  
pp. 631
Author(s):  
Sylvia Lee-Huang ◽  
Philip Lin Huang ◽  
Paul Lee Huang
Keyword(s):  
Nitric Oxide ◽  
Stem Cells ◽  
Stem Cell ◽  
Nitric Oxide Synthase ◽  
Real Time ◽  
Mitochondrial Biogenesis ◽  
Endothelial Nitric Oxide Synthase ◽  
Live Cell ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

We carried out live-cell real-time fluorescence imaging to follow the effects of genetic (siRNA) knockdown (KD) of endothelial nitric oxide synthase (eNOS) on mitochondrial biogenesis and adipogenesis in human mesenchymal stem cells (hMSCs). We report here that eNOS KD in hMSCs blocks mitochondrial biogenesis and adipogenesis. The transfer of mitochondria from normal hMSCs to eNOS-deficient hMSCs restores adipogenesis. Furthermore, cell-free mitochondria purified from normal hMSCs also restores adipogenesis in eNOS-deficient cells. Thus, eNOS and NO signaling are essential for mitochondrial biogenesis, and mitochondrial activity is indispensable for adipogenesis in hMSC differentiation. We mapped the path and identified the mechanisms of mitochondrial transfer. We captured real-time images of differentiated mature adipocytes in mitosis and replication. These results reveal that human stem cell-differentiated fat cells are capable of replication. This new finding offers novel insights into our understanding of fat cell expansion and the development of obesity. Real-time imaging in live cells allows synchronized investigation of mitochondrial biogenesis and adipogenesis in stem cell differentiation without reducing living cells to nonliving samples for functional analysis. Live-cell real-time imaging can thus be a faithful and immediate tool for molecular diagnostic medicine. Furthermore, our results suggest that mitochondrial remodeling can be a useful approach in treating adiposity, diabetes, and abnormalities in energy metabolism and vascular signaling.

Proinsulin C-peptide abrogates type-1 diabetes-induced increase of renal endothelial nitric oxide synthase in rats

2008 ◽  
Vol 24 (4) ◽  
pp. 331-338 ◽  
Author(s):  
Akihiro Kamikawa ◽  
Tatsuya Ishii ◽  
Kohei Shimada ◽  
Kennedy Makondo ◽  
Osamu Inanami ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Type 1 Diabetes ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
C Peptide ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide
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