Posttraumatic stress disorder (PTSD) is a growing public health concern. More recently, evidence has indicated that PTSD leads to obesity and associated metabolic dysfunction. Possible mechanisms of this link are through dysfunction of the hypothalamic-pituitary-adrenal axis and related moderation of appetite hormones and neural activity, leading to changes in consumptive behaviors. Although research has been examining associations between PTSD and obesity, diabetes, cardiovascular disease, and metabolic syndrome, future research should delineate potential mechanisms for these associations and develop targeted treatments to reduce these metabolic outcomes.
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http://dx.doi.org/10.1016/j.metabol.2014.08.009 | DOI Listing |
Stem Cell Rev Rep
January 2025
Institute of Stem Cell and Translational Cancer Research, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Human-induced pluripotent stem cell (hiPSC) technology has been applied in pathogenesis studies, drug screening, tissue engineering, and stem cell therapy, and patient-specific hiPSC-derived cardiomyocytes (hiPSC-CMs) have shown promise in disease modeling, including diabetic cardiomyopathy. High glucose (HG) treatment induces lipotoxicity in hiPSC-CMs, as evidenced by changes in cell size, beating rate, calcium handling, and lipid accumulation. Empagliflozin, an SGLT2 inhibitor, effectively mitigates the hypertrophic changes, abnormal calcium handling, and contractility impairment induced by HG.
View Article and Find Full Text PDFCurr Nutr Rep
January 2025
Faculty of Pharmaceutical Science, Assam down town University, Sankar Madhab Path, Gandhi Nagar, Panikhaiti, Guwahati, Assam, India, PIN - 781026.
Purpose Of Review: The term metabolic dysfunction-associated steatotic liver disease (MASLD) refers to a group of progressive steatotic liver conditions that include metabolic dysfunction-associated steatohepatitis (MASH), which has varying degrees of liver fibrosis and may advance to cirrhosis, and independent hepatic steatosis. MASLD has a complex underlying mechanism, with patients exhibiting diverse causes and phases of the disease. India has a pool prevalence of MASLD of 38.
View Article and Find Full Text PDFJ Gen Intern Med
January 2025
College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, United Arab Emirates.
Background: Type 2 diabetes mellitus (T2DM) and metabolic dysfunction-associated steatotic liver disease (MASLD), which have a reciprocal relationship compounded by obesity, are highly prevalent in the Middle East affecting morbidity, mortality, and healthcare costs.
Objective: This study aimed to assess the severity of MASLD and liver fibrosis among adult Emirati patients with long-standing T2DM.
Design And Participants: This cross-sectional study used noninvasive methods to assess the severity of MASLD and fibrosis progression in an adult cohort of Emirati patients (N = 546) with a mean T2DM duration of 16 years.
Mol Biol Rep
January 2025
Laboratory of Genomics and Human Genetics, Institut Pasteur du Maroc, Casablanca, Morocco.
Background: Male infertility (MI) is a polygenic condition mainly induced by spermatogenic failure/arrest or systemic disease with a large clinical spectrum. Lately, genetic sequencing allowed the identification of several variants implicated in both aforesaid situations.
Methods And Results: In this case study, we performed whole exome sequencing (WES) on the genomic DNA of a 37-year-old Moroccan man with Non-Obstructive Azoospermia.
Acta Neuropathol
January 2025
Department of Clinical Sciences, Lund Brain Injury Laboratory for Neurosurgical Research, Lund University, 222 20, Lund, Sweden.
Traumatic brain injury (TBI) often leads to impaired regulation of cerebral blood flow, which may be caused by pathological changes of the vascular smooth muscle cells (VSMCs) in the arterial wall. Moreover, these cerebrovascular changes may contribute to the development of various neurodegenerative disorders such as Alzheimer's-like pathologies that include amyloid beta aggregation. Despite its importance, the pathophysiological mechanisms responsible for VSMC dysfunction after TBI have rarely been evaluated.
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