Diabetic nephropathy is one the most serious diabetic microangiopathies, which is the main cause of mortality in diabetic patients. Our research investigated the protective effects of rutin on kidney of the type 1 diabetes mice induced by streptozotocin (STZ). The levels of kidney weight index (KWI), postprandial plasma glucose (PPG), creatinine (Cre), blood urine nitrogen (BUN), the activity of super oxide dismutase (SOD), malondialdehyde (MDA) and glutathione per oxidase (GSH-Px) were all measured. The histological morphology of kidney tissues was observed by hematoxylin-eosin (HE) staining, masson staining and electron microscope. The collagen I (COL-I) and transforming growth factor-β (TGF-β) levels were estimated by immunohistochemistry, western blot and Real-Time PCR respectively. The results revealed that the levels of SOD and GSH-Px all increased, while the levels of KWI, PPG, Cre, BUN and MDA all decreased in diabetic mice after the rutin treatment for eight weeks. Moreover, the histological morphology of kidney tissues was also improved. Furthermore, the expression of COL-I and TGF-β in kidney tissues increased significantly in the diabetic mice, which were antagonized by the rutin treatment. Together, the result suggested that rutin can improve kidney injury of the type 1 diabetic mice.
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Diabetes
January 2025
Department of Geriatrics, Peking University Shenzhen Hospital, Shenzhen, China.
Insulin resistance, a hallmark of type 2 diabetes, accelerates muscle breakdown and impairs energy metabolism. However, the role of Ubiquitin Specific Peptidase 2 (USP2), a key regulator of insulin resistance, in sarcopenia remains unclear. Peroxisome proliferator activated receptor γ (PPARγ) plays a critical role in regulating muscle atrophy.
View Article and Find Full Text PDFJ Am Soc Nephrol
January 2025
Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Background: Deficiency of adiponectin and its downstream signaling may contribute to the pathogenesis of kidney injury in type 2 diabetes. Adiponectin activates intracellular signaling via adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2), but the role of AdipoR-mediated signaling in glomerular injury in type 2 diabetes remains unknown.
Methods: The expression of AdipoR1 in the kidneys of people with type 2 diabetes and the expression of podocyte proteins or injury markers in the kidneys of AdipoR1-knockout (AdipoR1-KO) mice and immortalized AdipoR1-deficient human podocytes were investigated by immunohistochemistry and immunoblotting.
Am J Physiol Gastrointest Liver Physiol
January 2025
Digestive Diseases, Emory University, Atlanta, GA, United States.
The interplay between diet-induced obesity and gastrointestinal dysfunction is an evolving area of research with far-reaching implications for understanding the gutbrain axis interactions. In their study, Ramírez-Maldonado et al. employ a cafeteria (CAF) diet model to investigate the effects on gut microbiota, enteric nervous system (ENS) integrity and function, and gastrointestinal motility in mice.
View Article and Find Full Text PDFProtein synthesis is by far the most energetically costly cellular process in rapidly dividing cells. Quantifying translating ribosomes in individual cells and their average mRNA transit rate is arduous. Quantitating assembled ribosomes in individual cells requires electron microscopy and does not indicate ribosome translation status.
View Article and Find Full Text PDFInt J Cardiol Cardiovasc Risk Prev
March 2025
Beijing Chaoyang Hospital, Capital Medical University, Department of Endocrinology, Beijing, China.
Object: To explore the mechanism of diabetic cardiomyopathy that hyperglycemia may affect the cardiac function by inhibiting the expression of ATPase β subunit.
Method: Cardiac function, fibrosis levels, and the expression of the ATPase β subunit were observed in Akita mice-a diabetes mice model without lipid metabolism disorders--using morphological, molecular biology, and echocardiographic analyses compared to wild-type mice. The study revealed a connection between the decreased ATPase β subunit and the development of diabetic myocardial injury.
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