Background: The aetiopathogenesis of tendinopathy is uncertain, but inflammation may play a role in the early phase of tendinopathy and in tendon healing response. We investigated the most up-to-date evidence about the association between obesity, high-fat diet and tendinopathy, focusing on the role of adipokines, inflammatory pathways and molecular changes.
Sources Of Data: A systematic review was performed searching PubMed, Embase and Cochrane Library databases following the PRISMA guidelines. We included studies of any level of evidence published in peer-reviewed journals. The risk of bias (SIRCLE) was assessed, as was the methodological quality (CAMARADES) of the included studies. We excluded all the articles with a high risk of bias and/or low quality after the assessment. After applying the inclusion and exclusion criteria, we included 14 studies of medium or high quality.
Areas Of Agreement: A high-fat diet negatively affects tendon quality, increasing the risk of rupture and tendinopathy.
Areas Of Controversy: Controversial evidence exists on both tendon fat infiltration secondary to a dysregulation of the lipid metabolism and of a molecular effect of inflammatory pathways.
Growing Points: The secretion of adipokines is strictly related to fat ingestion and body composition and can potentially act on tendon physiology and injury.
Areas Timely For Developing Research: Adipokines, low-grade inflammation and fat intake play a role in disrupting tendon healing and setting up tendinopathy. Further high-quality research is needed to better define the molecular pathways involved.
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http://dx.doi.org/10.1093/bmb/ldab007 | DOI Listing |
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.
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Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
The incidence of type 2 diabetes has risen globally, in parallel with the obesity epidemic and environments promoting a sedentary lifestyle and low-quality diet. There has been scrutiny of ultra-processed foods (UPFs) as a driver of type 2 diabetes, underscored by their increasing availability and intake worldwide, across countries of all incomes. This narrative review addresses the accumulated evidence from investigations of the trends in UPF consumption and the relationship with type 2 diabetes incidence.
View Article and Find Full Text PDFExposure to toxins causes lasting damaging effects on the body. Numerous studies in humans and animals suggest that diet has the potential to modify the epigenome and these modifications can be inherited transgenerationally, but few studies investigate how diet can protect against negative effects of toxins. Potential evidence in the primary literature supports that caloric restriction, high-fat diets, high protein-to-carbohydrate ratios, and dietary supplementation protect against environmental toxins and strengthen these effects on their offspring's epigenome.
View Article and Find Full Text PDFJ Anat
January 2025
Hannover Medical School, Institute of Functional and Applied Anatomy, Hannover, Germany.
Obesity, along with hypoxia, is known to be a risk factor for pulmonary hypertension (PH), which can lead to right ventricular hypertrophy and eventually heart failure. Both obesity and PH influence the autonomic nervous system (ANS), potentially aggravating changes in the right ventricle (RV). This study investigates the combined effects of obesity and hypoxia on the autonomic innervation of the RV in a mouse model.
View Article and Find Full Text PDFBMC Pharmacol Toxicol
January 2025
Evangelical College, N'Djamena, BP 1200, Chad.
The study evaluated the anti-hyperlipidemic effects of myrcenol and curzerene on a high fat diet induced hyperlipidemia rat model. Thirty male albino rats were fed on a high-fat diet for four months. The HFD-induced hyperperlipidemia rats were treated with rosuvastatin (10 mg/kg), curzerene (130 mg/kg) and myrcenol (100 mg/kg) for four weeks.
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