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Palmitate potentiates the SMAD3-PAI-1 pathway by reducing nuclear GDF15 levels.
Cell Mol Life Sci
January 2025
Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Unitat de Farmacologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
Nuclear growth differentiation factor 15 (GDF15) reduces the binding of the mothers' against decapentaplegic homolog (SMAD) complex to its DNA-binding elements. However, the stimuli that control this process are unknown. Here, we examined whether saturated fatty acids (FA), particularly palmitate, regulate nuclear GDF15 levels and the activation of the SMAD3 pathway in human skeletal myotubes and mouse skeletal muscle, where most insulin-stimulated glucose use occurs in the whole organism.
View Article and Find Full Text PDFRole of transforming growth factor-β1 in regulating adipocyte progenitors.
Sci Rep
January 2025
Research Center for Pre-Disease Science, Faculty of Education and Research Promotion, University of Toyama, Toyama, 930-0194, Japan.
Adipose tissue (AT) metabolism involves coordinating various cells and cellular processes to regulate energy storage, release, and overall metabolic homeostasis. Therein, macrophage and its cytokine are important in controlling tissue homeostasis. Among cytokines, the role of transforming growth factor-β1 (Tgf-β1), a cytokine abundantly expressed in CD206 M2-like macrophage and correlated with the expansion of AT and fibrosis, in AT metabolism, remains unknown.
View Article and Find Full Text PDFPan-PPAR agonist lanifibranor improves insulin resistance and hepatic steatosis in patients with T2D and MASLD.
J Hepatol
January 2025
Division of Endocrinology, Diabetes and Metabolism, University of Florida, Gainesville, Florida, United States of America. Electronic address:
Background & Aims: Lanifibranor is a pan-PPAR agonist that improves glucose/lipid metabolism and reverses steatohepatitis and fibrosis in adults with MASH. We tested its effect on insulin resistance at the level of different target tissues in relationship to change in intrahepatic triglyceride (IHTG) content.
Methods: This phase 2, single center, study randomized (1:1) 38 patients with T2D and MASLD to receive lanifibranor 800 mg or placebo for 24 weeks.
Hepatic and Pancreatic Cellular Response to Early Life Nutritional Mismatch.
Endocrinology
January 2025
Department of Pediatrics, Divisions of Neonatology & Developmental Biology and Endocrinology, Neonatal Research Center of the UCLA Children's Discovery & Innovation Institute at the David Geffen School of Medicine at UCLA, Los Angeles, California 90095-1752.
To determine the basis for perinatal nutritional mismatch causing metabolic dysfunction associated steatotic liver disease (MASLD) and diabetes mellitus, we examined adult phenotype, hepatic transcriptome, and pancreatic β-islet function. In prenatal caloric restricted rat with intrauterine growth restriction (IUGR) and postnatal exposure to high fat with fructose (HFhf) or high carbohydrate (RC), we investigated male and female IUGR-Hfhf and IUGR-RC, versus HFhf and CON offspring. Males more than females displayed adiposity, glucose intolerance, insulin resistance, hyperlipidemia, hepatomegaly with hepatic steatosis.
View Article and Find Full Text PDFComparing the Effect of Heat Therapy and Mitochondrial-Targeted Antioxidants in Polycystic Ovarian Syndrome Phenotype Induced by Junk Food Consumption.
Reprod Sci
January 2025
Department of Physiology, Faculty of Medicine, Cairo University, Cairo, Egypt.
Polycystic ovarian syndrome (PCOS) is a complex endocrine-metabolic disorder, and multiple factors contribute to its pathophysiology. The current study assessed a PCOS-like animal model induced by consuming a high-fat sugar (HFHS) diet and compared the treatment outcome of mitochondrial-targeted antioxidants versus heat therapy. Sixty rats were divided into the following study groups: three control groups (negative and positive for the treatments used), HFHS, hot tub therapy (HTT) treatment, and MitoQ10 treatment (500 µmol/L MitoQ10 in clean drinking water daily, from week fourteen till week twenty-two of the study).
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