Hyperinsulinemia in newly diagnosed patients with multiple sclerosis

Abstract

There are limited data regarding glucose metabolism dysregulation in multiple sclerosis (MS). Present study investigates glucose and insulin response during oral glucose tolerance test (oGTT) in MS patients. We examined 19 MS patients and 19 age, sex and body mass index (BMI) matched healthy controls. MS patients were newly diagnosed, untreated and with low Expanded Disability Status Scale (EDSS) score (1.1 ± 0.7). Plasma glucose, lactate, insulin and GLP-1 during oGTT, and fasting adipokines, lipid and inflammatory parameters were analyzed. Insulin sensitivity indices (ISI) were calculated. MS patients had comparable fasting (5.2 ± 0.3 vs. 5.0 ± 0.4 mmol/l, p = 0.05) and post-load glucose concentrations as controls. Insulin response to oral glucose load in MS was increased (p = 0.022). Insulin sensitivity was lower in MS compared to controls [ISI(Matsuda) 6.95 ± 3.44 vs. 10.60 ± 4.81, p = 0.011 and ISI(Cederholm) 49.9 ± 15.3 vs. 61.3 ± 16.3, p = 0.032]. We did not find any difference in lactate, GLP-1, total, HDL and LDL cholesterol, triglycerides, interleukin 6, tumor necrosis factor, C-reactive protein, resistin, leptin, adiponectin levels between groups. We found decreased insulin sensitivity with postprandial hyperinsulinemia in MS patients, which seems not to be related to chronic inflammation or physical inactivity. The role of hyperinsulinemia in CNS function impairment should be further investigated.

Adiponectin profile at baseline is correlated to progression and severity of multiple sclerosis

“…Furthermore, through the secretion of adipokines, adipose tissue is strongly involved in the regulation of energy balance, insulin sensitization and immune response [33,34]. Among the adipokines, adiponectin, abundantly secreted in the serum, plays a significant role in autoimmune diseases although controversial results have been reported with regard to MS [22][23][24][25][26]. Very recently and in accordance with our results, the study of C ß oban et al [27] confirmed the involvement of adipokines in both the pathogenesis and progression of MS.…”

“…Until now, different studies have characterized total adiponectin in MS with controversial results . Recently, Çoban et al .…”

“…Until now, different studies have characterized total adiponectin in MS with controversial results [22][23][24][25][26]. Recently, C ß oban et al [27] found high levels of adiponectin and monocyte chemoattractant protein 1 (MCP-1) and suggested that they might potentially serve as prognostic biomarkers in MS.…”

Glucagon-Like Peptide-1 Analog, Liraglutide, Delays Onset of Experimental Autoimmune Encephalitis in Lewis Rats

“…Newly diagnosed MS patients exhibit hyperinsulinemia and decreased insulin sensitivity (Penesova et al, 2015) suggesting that obesity is a potential risk factor for MS (Palavra et al, 2016). Treating underlying metabolic syndrome with classic anti-diabetic drugs such as metformin and pioglitazone ameliorates metabolic disturbances, reduces MRI-evident lesion frequency and dampens T-cell pro-inflammatory response in MS patients (Negrotto et al, 2016).…”

Intracranial delivery of interleukin-17A via adeno-associated virus fails to induce physical and learning disabilities and neuroinflammation in mice but improves glucose metabolism through AKT signaling pathway

“…Recently, increased prevalence of insulin resistance and impaired glucose tolerance in MS patients was reported (Oliveira et al, 2014; Penesova et al, 2015; Wens et al, 2013). In previous studies, IL-17A inhibited adipogenesis and moderated adipose tissue accumulation in vitro and IL-17a −/− mice showed increased bodyweight, glucose tolerance and insulin sensitivity (Ahmed and Gaffen, 2010; Ahmed and Gaffen, 2013; Straus, 2013; Winer et al, 2009; Zuniga et al, 2010).…”