Role of Adipokines and Other Inflammatory Mediators in Gestational Diabetes Mellitus and Previous Gestational Diabetes Mellitus

Abstract

Previous Gestational Diabetes Mellitus (pGDM) is a common condition and has been associated with future development of Type 2 Diabetes Mellitus (T2DM) and Metabolic Syndrome (MS) in women affected. The pathogenesis and risk factors implicated in the development of these conditions later in the lives of women with pGDM are not as yet fully understood. Research has recently focused on a group of substances produced mainly by adipose tissue called adipokines, this group including, among others, adiponectin, leptin, Retinol-Binding Protein-4 (RBP-4), and resistin. These substances as well as other inflammatory mediators (CRP, IL-6, PAI-1, TNF-α) seem to play an important role in glucose tolerance and insulin sensitivity dysregulation in women with pGDM. We summarize the data available on the role of these molecules.

Ketotifen and Cardiovascular Risk in Patients with Type 2 Diabetes Mellitus

“…It's one of mast cell cytokine mediators [7,27]. This cytokine is increased in obesity and has multiple effects on insulin sensitivity in muscles, liver, or beta cells of the pancreas, ultimately leading to insulin resistance [26]. Our results showed that treatment with glimepiride plus ketotifen twice daily reverse obesity-related increases in IL-6 in obese patients with T2DM.…”

“…Interleukin-6 (IL-6) is inflammatory mediator produced by macrophages in the adipose tissue [26]. It's one of mast cell cytokine mediators [7,27].…”

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“…Combined with insulin resistance, chronic subclinical inflammation characterizes the hallmark pathway to the development of both gestational diabetes and gestational hypertension. 77-79 …”

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“…However, underlying pathophysiology of GDM in most instances is similar to that of type-2 DM, where the increased insulin resistance is converted into maternal hyperglycemia. The two main pathological mechanisms known to induce GDM involve the biochemical pathways leading to insulin resistance and chronic subclinical inflammation [5]. It has been suggested that prolonged stimulation of acute and chronic inflammation may be involved in the pathogenesis of insulin resistance [7].…”