ABSTRACT
YAN Y. LAM, CONNIE W. Y. HA, CRAIG R. CAMPBELL, ANDREW J. MITCHELL, ANUWAT DINUDOM, JAN OSCARSSON, DAVID I. COOK, NICHOLAS H. HUNT, IAN D. CATERSON, ANDREW J. HOLMES, AND LEN H. STORLIEN
4.1 INTRODUCTION
Visceral adiposity is strongly related to metabolic dysfunction including insulin resistance and systemic inflammation [1]–[3]. The deleterious metabolic effect of visceral fat is a consequence, in large part, of increased production of pro-inflammatory cytokines [4]. Adipose-derived immune factors primarily originate from cells in the stromal-vascular fraction of fat depots [5], [6]. Specifically, macrophage infiltration has been identified as a major determinant of the metabolic effect of adipose tissue. The abundance of macrophages in visceral fat was negatively correlated with
insulin sensitivity of obese individuals, whereas no such relationship was observed with subcutaneous fat [7]. The primary driver of the macrophage infiltration and pro-inflammatory profile of visceral fat, however, remains largely unknown.
