Abstract
BackgroundLeptin and adipocyte-fatty acid binding protein (A-FABP) are produced by white adipose tissue and may play a role in chronic inflammation in Multiple Sclerosis (MS). To assess leptin and A-FABP in relapsing and progressive forms of MS.MethodsAdipokine levels were measured in untreated adult relapsing-remitting MS (RRMS), secondary progressive MS (SPMS), primary progressive MS (PPMS) and Healthy control (HC). Pediatric-onset MS (POMS) and pediatric healthy controls (PHC) were also assessed. Leptin and A-FABP levels were measured in serum by ELISA. Groups were compared using linear mixed-effects model.ResultsExcluding two patients with Body Mass Index (BMI) > 50, a significant difference in leptin level was found between RRMS and HC controlling for age (p = 0.007), SPMS and HC controlling for age alone (p = 0.002), or age and BMI (p = 0.007). A-FABP levels were higher in SPMS than HC (p = 0.007), controlling for age and BMI. Differences in A-FABP levels between POMS and PHC was observed after controlling for age (p = 0.019), but not when BMI was added to the model (p = 0.081).ConclusionLeptin and A-FABP levels are highest in SPMS compared to HC, suggesting a role in pathogenesis of this disease subtype. A-FABP levels are increased in POMS patients and may play a role in the early stages of disease.
Highlights
Leptin and adipocyte-fatty acid binding protein (A-FABP) are produced by white adipose tissue and may play a role in chronic inflammation in Multiple Sclerosis (MS)
When the pairwise comparisons were investigated, leptin levels were significantly higher in SPMS compared to healthy controls (HC) (p = 0.003)
We found that A-FABP and leptin levels were significantly higher in SPMS patients with a body mass index (BMI) ≤ 50, compared to controls when adjusting for age and BMI
Summary
Leptin and adipocyte-fatty acid binding protein (A-FABP) are produced by white adipose tissue and may play a role in chronic inflammation in Multiple Sclerosis (MS). Multiple sclerosis (MS) is a T-cell mediated inflammatory disease, involving both innate and adaptive immunity [1]. Obesity has been associated with a chronic inflammatory state, due to the secretion of pro-inflammatory proteins in the blood [2]. A potential reason for the impact of obesity on disease is the associated increase in adipokines, a family of molecules with effects on inflammatory and autoimmune diseases [4]. Leptin is involved in the regulation of food-intake, energy expenditure, and inflammation. In addition to white adipose tissue (WAT), leptin is produced by lymphocytes [5,6].
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