Abstract
Metabolic syndrome (MS) presents with central obesity, impaired glucose metabolism, dyslipidemia and hypertension. Our aim was to examine the effect of metformin treatment either alone or in combination with non-steroidal anti-inflammatory drugs (NSAID) on plasma levels of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in patients with early stage MS (MS-es) and generalized MS (MS-ge). The study compared 35 female patients with MS-es (mean age of 43.39±1.54 years) and 40 patients with MS-ge (mean age of 45.69±2.18 years) to 10 age-matched controls each. Patients with MS-es were administered 850 mg metformin twice daily. The patients with MS-ge were divided into two groups of 20 patients per group. One group received metformin alone, while the other group received metformin in combination with 500 mg aspirin and 150 mg Diclac daily. Plasma NGF and BDNF levels were measured by ELISA. Statistical data analysis was performed using ANOVA. Plasma NGF and BDNF levels were significantly higher in MS-es patients and lower in MS-ge patients than in controls. NGF levels were decreased in both groups after treatment with metformin. NGF levels were significantly higher in MS-ge patients on combined therapy than in those on metformin only. The combination of metformin and NSAID treatment is more effective than metformin alone on NGF and BDNF production as well as on metabolism-related anthropometric and laboratory features. This represents a pathogenetic therapeutic mechanism in MS due to its strong anti-inflammatory effect and improves MS-ge symptoms.
Highlights
Metabolic syndrome (MS) is characterized by central obesity, impaired glucose metabolism, dyslipidemia and hypertension [1], insulin resistance [2] and high-sensitivity C-reactive protein (CRP) [3, 4]
Plasma nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) levels were significantly higher in MS-es patients and lower in MS-ge patients than in controls
NGF levels were decreased in both groups after treatment with metformin
Summary
Metabolic syndrome (MS) is characterized by central obesity, impaired glucose metabolism, dyslipidemia and hypertension [1], insulin resistance [2] and high-sensitivity C-reactive protein (CRP) [3, 4]. New pathophysiological data imply that MS is a real disease and its prevalence is increasing worldwide [7, 8]. MS presents with DM type 2 (DMT2) features, several cardiometabolic risk factors and increases in cardiovascular mortality [10]. Neurotrophins are signaling proteins discovered because of their prosurvival role in neuronal cells, and they mediate neurotrophic, immunotrophic and metabotropic effects [11]. Neurotrophins are considered key factors in MS pathogenesis, as any change in their plasma levels induces neuroendocrine-immune disturbances [15,16,17]
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