Somatostatin Receptor Expression in Peripheral Blood of Type 2 Diabetes Mellitus Patients

Introduction

Somatostatin, a peptide hormone released by neurons and secretory cells in the central and peripheral nervous system and in the gastrointestinal tract, has a broad inhibitory effect on the secretion of multiple pituitary, pancreatic and gastrointestinal hormones including growth hormone (GH), insulin and glucagon [1]. In addition, anti-inflammatory effects have been described, but data regarding the role of somatostatin in inflammation are controversial [2]. Effects of somatostatin are mediated through specific membrane somatostatin receptors (SSTR) that form a distinct group in the superfamily of G-protein coupled receptors. To date, five human receptor subtypes have been cloned [3], which can be considered to form two subfamilies, consisting of SSTR2, SSTR3, and SSTR5 making up one family, and SSTR1 and SSTR4 forming the second family [4].

Expression of specific SSTR subtypes has been demonstrated in peripheral blood cells [5], and pro-inflammatory cytokines like tumor necrosis factor alpha (TNF-α) can reduce SSTR expression levels [6]. Population-based studies have demonstrated that subclinical inflammation in the pathogenesis of T2DM is characterized by elevated serum levels of C-reactive protein, interleukin (IL)-6, TNF-α, and other immune mediators [7] [8]. Therefore, we tested the hypothesis that SSTR expression is down-regulated in peripheral blood cells from T2DM patients.

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