Guido Lastra is specialist in Internal Medicine and Endocrinology. He is a research-oriented assistant professor at the University of Missouri in Columbia. His area of interest is the pathogenesis of chronic over-nutrition induced insulin resistance and cardiovascular disease. He is focused on studying the role of the mineralocorticoid receptor in the development of insulin resistance-mediated vascular dysfunction. In particular, he is actively exploring the interactions between inflammation and mineralocorticoid receptor activation that lead to vascular stiffness. Dr. Lastra has presented his research in several prestigious International conferences, including the International Aldosterone Conference, the Endocrine Society Meeting, and the American Heart association (High Blood Pressure Council) Meeting. Dr. Lastra has more than 50 publications in peer-reviewed journals, frequently as first author, in prestigious journals including, Diabetes, Endocrinology, Hypertension, and the American Journal of Physiology (AJP). He has served as reviewer for important journals, including Diabetes, Diabetes Care, and the Lancet. 


Obesity is a leading risk factor for the development of type 2 diabetes mellitus (DM2) and cardiovascular disease (CVD), however the underlying mechanisms still remain to be fully uncovered. It is now well accepted that dysfunctional adipose tissue in conditions of obesity is a critical source of inflammation that impacts the cardiovascular system and contributes to CVD. Although traditionally visceral adipose tissue has been linked to increased CVD risk, there is mounting interest in the role that fat accumulation around the vasculature plays in the pathogenesis of vascular dysfunction. Perivascular adipose tissue – PVAT- is in intimate contact with large, medium and small diameter arterial beds in several tissues, and has been shown to control vascular function as well as remodeling. PVAT does not merely mirror visceral adipose tissue changes seen in obesity, but has unique features that impact vascular biology. In lean individuals PVAT exerts vasodilatory and anti-inflammatory functions, however obesity results in PVAT inflammation, characterized by imbalance between pro and anti- inflammatory cells as wells as adipokines. PVAT inflammation promotes insulin resistance in the vasculature, thus resulting in impaired insulin-mediated vasodilatory responses and vascular remodeling. In this review we address current knowledge about the mechanisms that link PVAT inflammation to insulin resistance and vascular dysfunction. Indeed, PVAT emerges as a novel type of adipose tissue that participates in the pathogenesis of CVD, independently to a large extent to visceral adipose tissue.



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