Metabolic syndrome is a multifactorial disease with high prevalence worldwide. It is related to cardiovascular disease, diabetes, and obesity. Approximately 80% of patients with metabolic syndrome have some degree of fatty liver disease. An adenosine derivative (IFC-305) has been shown to exert protective effects in models of liver damage as well as on elements involved in central metabolism; therefore, here, we evaluated the effect of IFC-305 in an experimental model of metabolic syndrome in rats induced by a high-fat diet and 10% sucrose in drinking water for 18 weeks. We also determined changes in fatty acid uptake in the Huh-7 cell line. In the experimental model, increases in body mass, serum triglycerides and proinflammatory cytokines were induced in rats, and the adenosine derivative significantly prevented these changes. Interestingly, IFC-305 prevented alterations in glucose and insulin tolerance, enabling the regulation of glucose levels in the same way as in the control group. Histologically, the alterations, including mitochondrial morphological changes, observed in response to the high-fat diet were prevented by administration of the adenosine derivative. This compound exerted protective effects against metabolic syndrome, likely due to its action in metabolic regulation, such as in the regulation of glucose blood levels and hepatocyte fatty acid uptake.
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Department of Rehabilitation, Jiujiang College Hospital, Jiujiang, Jiangxi, China.
Metabolic diseases have gradually become one of the most significant global medical burdens. Diseases such as obesity, diabetes, and metabolic syndrome, along with their complications, are clinically categorized as metabolic diseases. Long-term oral medication significantly reduces patient compliance and quality of life.
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Department of Endocrinology and Metabolism, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang, China.
Short stature, joint hyperextension, ocular hypotension, Rieger abnormalities, and delayed tooth eruption (SHORT) syndrom is a rare primary autosomal dominant genetic disorder mainly caused by pathogenic loss-of-function variants in the phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1) gene. We report the case of a Chinese adult female patient with SHORT syndrome, carrying a PIK3R1 gene variant (c.1945C > T), who developed abnormal glucose metabolism and severe postprandial insulin resistance over 9 years.
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Clinical and Research Infectious Diseases Department, National Institute for Infectious Diseases Lazzaro Spallanzani Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy.
The pathogenesis of long COVID (LC) still presents many areas of uncertainty. This leads to difficulties in finding an effective specific therapy. We hypothesize that the key to LC pathogenesis lies in the presence of chronic functional damage to the main anti-inflammatory mechanisms of our body: the three reflexes mediated by the vagus nerve, the hypothalamic-pituitary-adrenal (HPA) hormonal axis, and the mitochondrial redox status.
View Article and Find Full Text PDFJ Diabetes Metab Disord
June 2025
Aragón Health Research Institute, University of Zaragoza Faculty of Medicine, Domingo Miral s/n, Zaragoza, 50009 Spain.
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Cureus
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Department C, National Institute of Nutrition of Tunis, Tunis, TUN.
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