Objective: To evaluate the role oral administration of S-nitroso-N-acetylcysteine (SNAC), a NO donor drug, in the prevention and reversion of NASH in two different animal models.
Methods: NASH was induced in male ob/ob mice by methionine-choline deficient (MCD) and high-fat (H) diets. Two animal groups received or not SNAC orally for four weeks since the beginning of the treatment. Two other groups were submitted to MCD and H diets for 60 days receiving SNAC only from the 31(st) to the 60(th) day.
Results: SNAC administration inhibited the development of NASH in all groups, leading to a marked decrease in macro and microvacuolar steatosis and in hepatic lipid peroxidation in the MCD group. SNAC treatment reversed the development of NASH in animals treated for 60 days with MCD or H diets, which received SNAC only from the 31(st) to the 60(th) day.
Conclusions: Oral administration of SNAC markedly inhibited and reversed NASH induced by MCD and H diets in ob/ob mice.
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http://dx.doi.org/10.1080/07315724.2008.10719703 | DOI Listing |
J Endocrinol
January 2025
U Iwaniec, Skeletal Biology Laboratory, Oregon State University, Corvallis, United States.
Leptin increases focal inflammation and osteolysis induced by polyethylene particles in leptin-deficient ob/ob mice suggesting the adipokine, an important immune modulator, contributes to orthopedic implant failure. Focal inflammation leads to bone loss at distant skeletal sites, and it is plausible that leptin also contributes to this response. We tested this possibility in 6-week-old female ob/ob mice (6-8/group) by evaluating bone architecture, turnover, and gene expression 12 days following surgical placement of polyethylene particles over calvaria.
View Article and Find Full Text PDFGenes (Basel)
December 2024
Zhejiang Key Laboratory of Medical Epigenetics, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Background/objectives: UFMylation, a newly identified ubiquitin-like modification, modulates a variety of physiological processes, including endoplasmic reticulum homeostasis maintenance, DNA damage response, embryonic development, and tumor progression. Recent reports showed that UFMylation plays a protective role in preventing liver steatosis and fibrosis, serving as a defender of liver homeostasis in the development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the regulation of UFMylation in MASLD remains unclear.
View Article and Find Full Text PDFRedox Biol
January 2025
Department of Anatomy and Convergence Medical Science, College of Medicine, Metabolic Dysfunction Liver Disease Research Center, Institute of Medical Science, Gyeongsang National University, Jinju, 52727, Republic of Korea. Electronic address:
Although leptin-deficient ob/ob mice have been investigated to determine whether hepatic steatosis promotes susceptibility to hepatotoxic insults, carbon tetrachloride (CCl)-induced hepatic fibrosis in ob/ob mice remains largely unknown. In this study, we evaluate the pathogenic mechanisms of hepatic fibrosis in CCl-treated wild-type (WT) and ob/ob mice and analyze some parameters related to lipogenesis, inflammation, fibrosis, oxidative stress, apoptosis, and autophagy. CCl treatment attenuated liver weight and lipogenesis in ob/ob mice.
View Article and Find Full Text PDFJ Nutr Biochem
January 2025
Faculty of Health, Southern Cross University, Gold Coast, QLD, 4225, Australia. Electronic address:
Glutamine availability may be reduced in chronic diseases, such as type 2 diabetes mellitus (T2DM)-induced by obesity. Herein, the antioxidant, anti-inflammatory and lipid metabolism effects of chronic oral glutamine supplementation in its free and dipeptide form were assessed in ob/ob mice. Adult male C57BL/6J ob/ob mice were supplemented with L-alanyl-L-glutamine (DIP) or free L-glutamine (GLN) in the drinking water for 40 days, whilst C57BL/6J Wild-type lean (WT) and control ob/ob mice (CTRL) received fresh water only.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Department of Anatomy, Chonnam National University Medical School, Hwasun 58128, Republic of Korea; Biomedical Science Graduate Program (BMSGP), Chonnam National University, Hwasun 58128, Republic of Korea. Electronic address:
Obesity is a prevalent metabolic disorder linked to insulin resistance, hyperglycemia, increased adiposity, chronic inflammation, and cognitive dysfunction. Recent research has focused on developing therapeutic strategies to mitigate cognitive impairment associated with obesity. Insulin growth factor-1 (IGF1) deficiency is linked to insulin resistance, glucose intolerance, and the progression of obesity-related central nervous system (CNS) disorders.
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