Methods: Male C57BL/6J mice were randomly divided into six different experimental groups (8 animals/group): (1) normal group (NOR), (2) normal control group (NC), (3) normal + exercise group (NE), (4) IGT group (IGT), (5) IGT control group (IC), and (6) IGT+ exercise group (IE).The exercise group received aerobic exercise for 8 weeks. After the intervention, a blood glucose meter was used to detect the level of glucose tolerance in the mouse's abdominal cavity; a biochemical kit was used to detect serum lipid metabolism indicators, malondialdehyde, and superoxide dismutase levels; the ELISA method was used to detect serum insulin and mouse gastrocnemius homogenate LDH, PDH, SDH, and CCO levels. Western blot method was used to detect the protein expression levels of NOX4, PGC-1, and Mfn2 in the gastrocnemius muscle of mice.
Results: (1) Mice with high-fat diet for 30 weeks showed impaired glucose tolerance, insulin resistance, and lipid metabolism disorders. The level of LDH, PDH, SDH, and CCO in the gastrocnemius homogenate of mice was reduced. The expressions of NOX4 protein were significantly upregulated, while the expressions of PGC-1 and Mfn2 proteins were significantly downregulated. (2) 8-week aerobic exercise improved the disorders of glucose and lipid metabolism in IGT mice and increased homogenized LDH, PDH, SDH, and CCO levels, and the expressions of NOX4, PGC-1, and Mfn2 proteins in the gastrocnemius muscle of mice were reversed. It is speculated that aerobic exercise can accelerate energy metabolism.
Conclusion: (1) C57BL/6 mice were fed high fat for 30 weeks and successfully constructed a mouse model of reduced diabetes; the mice with reduced diabetes have impaired glucose tolerance, insulin resistance, and lipid metabolism disorders; (2) 8 weeks of aerobic exercise improve glucose tolerance, reduce glucose tolerance in mice, reduce insulin resistance, improve lipid metabolism disorders, and reduce oxidative stress; (3) 8-week aerobic exercise reduces skeletal muscle NOX4 expression and increases glucose tolerance; reduces the expression of LDH, PDH, SDH, and CCO in mouse skeletal muscle; increases the expression level of mitochondrial fusion protein 2 and PGC-1; improves glucose tolerance; reduces energy metabolism of mouse skeletal muscle; reduces oxidative stress; and reduces insulin resistance. It is speculated that aerobic exercise can accelerate energy metabolism. This process may involve two aspects: firstly, increase the expression level of oxidative metabolism enzymes and promote the tricarboxylic acid cycle; secondly, increase the expression of Mfn2 and accelerate mitochondria fission or fusion to regulate energy metabolism, thereby reducing oxidative stress and insulin resistance.
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http://dx.doi.org/10.1155/2022/3780156 | DOI Listing |
Diabetes Obes Metab
January 2025
Department of Medicine, Division of Endocrinology, Diabetes Research Center, Columbia University Irving Medical Center, New York, New York, USA.
Objective: Post-prandial glucose response (PPGR) is a risk factor for cardiovascular disease. Meal carbohydrate content is an important predictor of PPGR, but dietary interventions to mitigate PPGR are not always successful. A personalized approach, considering behaviour and habitual pattern of glucose excursions assessed by continuous glucose monitor (CGM), may be more effective.
View Article and Find Full Text PDFProg Cardiovasc Dis
December 2024
Saint Luke's Mid America Heart Institute and University of Missouri-Kansas City, Kansas City, MO, United States of America.
American culture encourages overconsumption, fueled by ubiquitous availability and pervasive marketing of ultra-processed foods and other addictive substances. This chronic overindulgence has contributed to rising rates of obesity, type 2 diabetes (T2D), substance abuse, mental health disorders and premature mortality. Glucose-like peptide-1 agonists (GLP-1RAs) affect the brain's reward pathway that mediates addiction to foods and various other substances.
View Article and Find Full Text PDFBone
December 2024
Marrow Adiposity and Bone Lab, MABLab-ULR4490, Univ. Littoral Côte d'Opale F-62200 Boulogne-sur-Mer, Univ. Lille F-59000 Lille, CHU Lille, F-59000 Lille, France. Electronic address:
Obesity is a risk factor of developing type 2 diabetes (T2D) and metabolic complications, through systemic inflammation and insulin resistance. It has also been associated with increased bone marrow adipocytes along with increased bone fragility and fracture risk. However, the differential effects of obesity and T2D on bone fragility remain unclear.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Islet Biology and Metabolism Lab - IBM Lab, Department of Physiological Sciences, Center of Biological Sciences, Federal University of Santa Catarina - UFSC, Florianópolis, Santa Catarina, Brazil.
Aims: This study investigates the role of Hepatocyte Nuclear Factor 4α (HNF4α) in the adaptation of pancreatic β-cells to an HFD-induced obesogenic environment, focusing on β cell mass expansion and metabolic adaptations.
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Cureus
November 2024
Community Medicine, Baba Raghav Das Medical College, Gorakhpur, IND.
Background Thalassemia is the most common form of hereditary anemia caused by the impaired synthesis of one of the two globin chains in hemoglobin. A decrease in beta-globin chains occurs in beta-thalassemia, resulting in a relative excess of alpha-globin chains. Thalassemia major is the severe form of thalassemia, which requires frequent blood transfusions for survival.
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