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Review
- Regulation of Muscle Microcirculation in Health and Diabetes
- Zhenqi Liu, Seung-Hyun Ko, Weidong Chai, Wenhong Cao
- Diabetes Metab J. 2012;36(2):83-89. Published online April 17, 2012
- DOI: https://doi.org/10.4093/dmj.2012.36.2.83
- 3,583 View
- 31 Download
- 7 Crossref
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Abstract
PDF
PubReader Insulin increases microvascular perfusion and substrate exchange surface area in muscle, which is pivotal for hormone action and substrate exchange, by activating insulin signaling cascade in the endothelial cells to produce nitric oxide. This action of insulin is closely coupled with its metabolic action and type 2 diabetes is associated with both metabolic and microvascular insulin resistance. Muscle microvascular perfusion/volume can be assessed by 1-methylxanthine metabolism, contrast-enhanced ultrasound and positron emission tomography. In addition to insulin, several factors have been shown to recruit muscle microvasculature, including exercise or muscle contraction, mixed meals, glucagon-like peptide 1 and angiotensin II type 1 receptor (AT1R) blocker. On the other hand, factors that cause metabolic insulin resistance, such as inflammatory cytokines, free fatty acids, and selective activation of the AT1R, are capable of causing microvascular insulin resistance. Therapies targeting microvascular insulin resistance may help prevent or control diabetes and decrease the associated cardiovascular morbidity and mortality.
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Citations
Citations to this article as recorded by
- Cardiovascular aging and the microcirculation of skeletal muscle: using contrast-enhanced ultrasound
Emily C. Dunford, Jason S. Au, Michaela C. Devries, Stuart M. Phillips, Maureen J. MacDonald
American Journal of Physiology-Heart and Circulatory Physiology.2018; 315(5): H1194. CrossRef - Direct Activation of Angiotensin II Type 2 Receptors Enhances Muscle Microvascular Perfusion, Oxygenation, and Insulin Delivery in Male Rats
Fei Yan, Zhaoshun Yuan, Nasui Wang, Robert M Carey, Kevin W Aylor, Li Chen, Xinmin Zhou, Zhenqi Liu
Endocrinology.2018; 159(2): 685. CrossRef - Long-term high-fat diet induces hippocampal microvascular insulin resistance and cognitive dysfunction
Zhuo Fu, Jing Wu, Tanseli Nesil, Ming D. Li, Kevin W. Aylor, Zhenqi Liu
American Journal of Physiology-Endocrinology and Metabolism.2017; 312(2): E89. CrossRef - GLP-1 Receptor Agonist Exenatide Increases Capillary Perfusion Independent of Nitric Oxide in Healthy Overweight Men
Mark M. Smits, Marcel H.A. Muskiet, Lennart Tonneijck, Mark H.H. Kramer, Michaela Diamant, Daniël H. van Raalte, Erik H. Serné
Arteriosclerosis, Thrombosis, and Vascular Biology.2015; 35(6): 1538. CrossRef - New insights into insulin action and resistance in the vasculature
Camila Manrique, Guido Lastra, James R. Sowers
Annals of the New York Academy of Sciences.2014; 1311(1): 138. CrossRef -
Angiotensin-(1–7) Recruits Muscle Microvasculature and Enhances Insulin’s Metabolic Action via
Mas
Receptor
Zhuo Fu, Lina Zhao, Kevin W. Aylor, Robert M. Carey, Eugene J. Barrett, Zhenqi Liu
Hypertension.2014; 63(6): 1219. CrossRef - Insulin Resistance and Skeletal Muscle Vasculature: Significance, Assessment and Therapeutic Modulators
Camila Manrique, James R. Sowers
Cardiorenal Medicine.2014; 4(3-4): 244. CrossRef
- Cardiovascular aging and the microcirculation of skeletal muscle: using contrast-enhanced ultrasound
Original Article
- Mechanism of Impaired Endothelium-dependent Vasodilation in Otsuka Long-Evans Tokushima Fatty (OLETF) Rats .
- Kook Jin Chun, Seok Man Son, In Ju Kim, Chi Dae Kim, Seok Dong Yoo, Yong Ki Kim
- Korean Diabetes J. 2002;26(1):47-57. Published online February 1, 2002
- 921 View
- 17 Download
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Abstract
PDF
- BACKGROUND
Impaired vascular endothelium-dependent relaxation and augmented contractile responses have been reported in several long-term animals hyperglycemia models and human diabetic patients. Since oxidative stress has been implicated as a contributor to impaired vascular function, the mechanism of an impaired endothelium-dependent vasodilation in Otsuka Long-Evans Tokushima Fatty (OLETF) rats was investigated. METHODS: This present study was undertaken to characterize both the vascular production and the enzymatic source of the superoxide anion in the type 2 diabetic rats. RESULTS: In the thoracic aortas of OLETF rats, endothelium-dependent relaxation was markedly attenuated compared to that of the control rats (LETO, Long-Evans Tokushima Otsuka) in association with a significant increase in superoxide production (2421.39+/-07.01 nmol/min/mg). There was no difference in eNOS expression between the OLETF rats and LETO rats. The increased production of superoxide anion was significantly attenuated by diphenyleneiodonium (DPI, 10 mol/L), NAD (P)H oxidase inhibitor. In line with these results, studies using various enzyme inhibitors such as DPI, allopurinol, rotenone and L-NMMA suggest that the main source of superoxide anions in the aorta is NAD (P)H oxidase. CONCLUSION: These results suggest that enhanced NAD(P)H oxidase activity and reduced nitric oxide (NO) availability through an interaction between NO and superoxide anion contribute to the impaired endothelium-dependent vasodilation in OLETF rats.
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