In this study, in order to clarify the kinetics of leptin, we focused on the ratio of leptin concentrations in cerebrospinal fluid and serum in aged male rats, and examined the weight of epididymal fat, and the passage rate of leptin through the blood-brain barrier. In the lighter animals, the epididymal fat weight was low, while leptin concentrations in the serum and cerebrospinal fluid were also low. Conversely, in the heavier animals, the weight of epididymal fat and leptin concentrations in the serum and cerebrospinal fluid were higher. With regard to the ratio of leptin in the cerebrospinal fluid and serum, the passage rate of leptin through the blood-brain barrier was lower in the heavier animals than in the lighter animals.
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http://dx.doi.org/10.1538/expanim.57.485 | DOI Listing |
J Vet Sci
December 2024
Laboratory of Developmental Biology and Genomics, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Importance: The brain and adipose tissue interact metabolically, and if there is a problem with the energy metabolism of the brain, it cannot maintain the energy balance with the adipose tissue. Therefore, when adenylate kinase 5 (), which regulates energy metabolism in the brain, is knocked out, problems with lipid metabolism may occur.
Objective: We aimed to elucidate the metabolic function and phenotype of , a gene with an unknown function in metabolism.
Diabetes Obes Metab
January 2025
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Engineering Research Center for Dental Materials and Advanced Manufacture, Department of Anesthesiology, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Background: Given the potential role of brown adipose tissue (BAT) in stimulating energy expenditure, activating BAT can be an effective anti-obesity treatment. Here, we aimed to use adenoviruses to establish the effect of the inducible degrader of the low density lipoprotein receptor (IDOL) in the formation of BAT.
Methods: IDOL or green fluorescent protein was overexpressed by adenovirus and injected into the scapula of C57BL/6J mice and fed with high-fat diet for 12 weeks.
Am J Physiol Regul Integr Comp Physiol
January 2025
College of Sport and Health, Shandong Sport University, Jinan, Shandong, 250102, China.
Obesity can change the immune microenvironment of adipose tissue and induce inflammation. This study is dedicated to exploring the internal mechanism by which different intensities of exercise reprogram the immune microenvironment of epididymal adipose tissue in nutritionally obese mice. C57BL/6J male obese mouse models were constructed by high-fat diet, which were respectively obese control group (OC), moderate intensity continuous exercise group (HF-M), high intensity continuous exercise group (HF-H) and high intensity intermittent exercise group (HF-T).
View Article and Find Full Text PDFMicrobiome Res Rep
July 2024
Department of Biomedical Sciences, Carson College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331, USA.
The gut microbiota has been implicated as a major factor contributing to metabolic diseases and the response to drugs used for the treatment of such diseases. In this study, we tested the effect of cholestyramine, a bile acid sequestrant that reduces blood cholesterol, on the murine gut microbiota and metabolism. We also explored the hypothesis that some effects of this drug on systemic metabolism can be attributed to alterations in the gut microbiota.
View Article and Find Full Text PDFRedox Biol
December 2024
Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA, USA; Department of Biomedical Engineering, UAB, Birmingham, AL, USA. Electronic address:
Background: Diabetes increases ischemic heart injury via incompletely understood mechanisms. We recently reported that diabetic adipocytes-derived small extracellular vesicles (sEV) exacerbate myocardial reperfusion (MI/R) injury by promoting cardiomyocyte apoptosis. Combining in vitro mechanistic investigation and in vivo proof-concept demonstration, we determined the underlying molecular mechanism responsible for diabetic sEV-induced cardiomyocyte apoptosis after MI/R.
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