Adela Penesova has completed her PhD in 2006 (Comenius University in Bratislava, Slovakia) and she was a Post-doctoral fellow at Obesity and Diabetes Clinical\r\nResearch Section, National Institute of Diabetes & Digestive & Kidney Diseases, National Institute of Health (NIH), Phoenix, AZ, USA. She is a Senior Scientist in a\r\nCenter of Molecular medicine, SAS, and teacher for Faculty of Medicine, Slovak Medical University in Bratislava, Slovakia. She has published more than 33 papers\r\nin reputed journals and has been serving as an Editorial Board Member of repute for Endocrine Regulation.
Insulin also plays a role in neuron growth, neuroplasticity, and neuro modulation. It has been hypothesized that in vivo\r\nimpaired insulin functions may be involved in pathogenesis of demyelinating disease. There are limited data regarding\r\nglucose metabolism dysregulation in multiple sclerosis (MS). Present study investigates glucose and insulin metabolism in\r\nnewly diagnosed MS patients in association to inflammatory markers. We examined 19 MS patients and 19 age, sex and body\r\nmass index (BMI) matched healthy controls. MS patients were newly diagnosed, untreated and with low Expanded Disability\r\nStatus Scale (EDSS) score (1.1±0.7). Plasma glucose, lactate, insulin and GLP-1 were measured during oral glucose tolerance\r\ntest. Fasting adipokines, lipid and inflammatory parameters were analyzed. Insulin sensitivity indices (ISI) were calculated.\r\nMS patients had comparable fasting and post-load glucose concentrations as controls. Insulin response to oral glucose load\r\nin MS was increased (p=0.022). Insulin sensitivity was lower in MS compared to controls [ISI (Matsuda) p=0.011 and ISI\r\n(Cederholm) p=0.032]. We did not find any difference in inflammatory parameters (interleukin 6, tumor necrosis factor,\r\nC-reactive protein), nor in lactate, GLP-1, total, HDL and LDL cholesterol, triglycerides, resistin, leptin, adiponectin levels\r\nbetween groups. We found decreased insulin sensitivity with postprandial hyperinsulinemia in MS patients, which seems not\r\nto be related to chronic inflammation or physical inactivity. The role of hyperinsulinemia in CNS function impairment and\r\ninsulin sensitizing therapy for better remyelination repair should be further investigated.
Gerald Dieter Griffin has an extensive background in clinical and basic research as well as in clinical medicine. In addition to his medical practice he currently\r\nconducts clinical research on traumatic brain injury and offers his services as a consultant to various biotechnology companies. His specific research interests include\r\nTBI, the immune response and infection in TBI/stroke, the molecular/immune events of PTSD and treatments. He is retired from the Army giving more than 40 years\r\nof distinguished service as an Active Duty and Army Reserve Soldier. As such, he has extensive knowledge of research being conducted in a military setting.
Several themes supported by a robust literature are addressed in this clinical translational review and research paper: The\r\ninadequate standard of care for minimal Traumatic Brain Injury (mTBI)/concussion when compared to stroke because\r\ndiagnosis and care for mTBI/concussion are based primarily on a symptom only framework; the treatment of stroke (brain\r\ninjury) with select antibiotics; the use of beta blockade in stroke (brain injury). The various etiologies of brain injury appear\r\nto coalesce to common endpoints: Potential neuronal demise, cognitive and functional losses, immune suppression and\r\ninfection. The use of principles patterned after ‘Koch’s Postulates’ (show/prove the presence of infection/illness/disease, treat\r\nuntil resolved appears to be marginalized in establishing a diagnosis and recovery from mTBI/TBI. The pathways of immune\r\nsystem interactions in stroke (brain injury) and infection are briefly discussed. The suggestion of combined specific antibiotic\r\nand beta blockade for ischemic stroke (brain injury) and mTBI is advanced for treatment and expeditious further study. Stroke\r\nis considered a brain injury in this paper. Stroke is also considered and recommended as a study model for mTBI therapy\r\nbecause of their common end points from brain damage. It is suggested that potential transfer or translation of therapy for\r\nstroke may be useful in mTBI.