PMID- 20098632 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20211020 IS - 1937-9080 (Print) IS - 1937-9080 (Electronic) IS - 1937-9080 (Linking) VI - 1 IP - 2 DP - 2009 Apr 1 TI - Regulation of Microvascular Function by Adipose Tissue in Obesity and Type 2 Diabetes: Evidence of an Adipose-Vascular Loop. PG - 133 AB - In recent years, the general concept has emerged that chronic low-grade inflammation is the condition linking excessive development of adipose tissue and obesity-associated pathologies such as type 2 diabetes and cardiovascular diseases. Obesity and type 2 diabetes are characterized by a diminished production of protective factors such as adiponectin and increased detrimental adipocytokines such as leptin, resistin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNFalpha), and monocyte chemoattractant protein-1 (MCP-1) by adipose tissue. Moreover, the evidence that the growth of the fat mass is associated with an accumulation of adipose tissue macrophages and T-lymphocytes has raised the hypothesis that the development of an inflammatory process within the growing fat mass is a primary event involved in the genesis of systemic metabolic and vascular alterations. This crosstalk of adipocyte, macrophage, lymphocyte, endothelial cells, and vascular smooth muscle cells contribute to the production of various cytokines, chemokines, and hormone-like factors, which actively participate in the regulation of vascular function by an endocrine and/or paracrine pattern. Thus, the signaling from perivascular adipose to the blood vessels is emerging as a potential therapeutic target for obesity and diabetes-associated vascular dysfunction. FAU - Zhang, Hanrui AU - Zhang H AD - Departments of Internal Medicine, Medical Pharmacology & Physiology and Nutritional Sciences, Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, MO 65211. FAU - Zhang, Cuihua AU - Zhang C LA - eng GR - R01 HL077566-01A2/HL/NHLBI NIH HHS/United States GR - R01 HL077566/HL/NHLBI NIH HHS/United States GR - R01 HL077566-03/HL/NHLBI NIH HHS/United States GR - R01 HL085119-01A1/HL/NHLBI NIH HHS/United States GR - R01 HL085119-03/HL/NHLBI NIH HHS/United States GR - R01 HL085119/HL/NHLBI NIH HHS/United States GR - R01 HL077566-02/HL/NHLBI NIH HHS/United States GR - R01 HL085119-04/HL/NHLBI NIH HHS/United States GR - R01 HL085119-02/HL/NHLBI NIH HHS/United States PT - Journal Article PL - United States TA - Am J Biomed Sci JT - American journal of biomedical sciences JID - 101515147 PMC - PMC2809393 MID - NIHMS99789 EDAT- 2010/01/26 06:00 MHDA- 2010/01/26 06:01 PMCR- 2010/01/21 CRDT- 2010/01/26 06:00 PHST- 2010/01/26 06:00 [entrez] PHST- 2010/01/26 06:00 [pubmed] PHST- 2010/01/26 06:01 [medline] PHST- 2010/01/21 00:00 [pmc-release] AID - 10.5099/aj090200133 [doi] PST - ppublish SO - Am J Biomed Sci. 2009 Apr 1;1(2):133. doi: 10.5099/aj090200133.