Leuconostoc mesenteroides subsp. mesenteroides SD23 Prevents Metabolic Dysfunction Associated with High-Fat Diet–Induced Obesity in Male Mice

2019 ◽  
Vol 12 (2) ◽  
pp. 505-516 ◽  
Author(s):  
Diana C. Castro-Rodríguez ◽  
Luis A. Reyes-Castro ◽  
Claudia C. Vega ◽  
Guadalupe L. Rodríguez-González ◽  
Jorge Yáñez-Fernández ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Leuconostoc Mesenteroides ◽  
Metabolic Dysfunction ◽  
Male Mice ◽  
High Fat ◽  
Diet Induced Obesity

Therapeutic effects of açaí seed extract on hepatic steatosis in high‐fat diet‐induced obesity in male mice: a comparative effect with rosuvastatin

2020 ◽  
Vol 72 (12) ◽  
pp. 1921-1932
Author(s):  
Thamires Barros Tavares ◽  
Izabelle Barcellos Santos ◽  
Graziele Freitas Bem ◽  
Dayane Teixeira Ognibene ◽  
Ana Paula Machado Rocha ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Seed Extract ◽  
Therapeutic Effects ◽  
Male Mice ◽  
High Fat ◽  
Comparative Effect ◽  
Diet Induced Obesity

SIRT6 in mouse spermatogenesis is modulated by diet-induced obesity

2011 ◽  
Vol 23 (7) ◽  
pp. 929 ◽  
Author(s):  
Nicole O. Palmer ◽  
Tod Fullston ◽  
Megan Mitchell ◽  
Brian P. Setchell ◽  
Michelle Lane
Keyword(s):  
Dna Damage ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Control Diet ◽  
Male Mice ◽  
High Fat ◽  
Sperm Dna Damage ◽  
Diet Induced Obesity ◽  
Damage Repair ◽  
Sperm Dna

Male obesity is associated with reduced sperm function and increased incidence of sperm DNA damage; however, the underlying molecular mechanisms have not yet been identified. Mammalian SIRT6 protein is involved in caloric-dependant DNA damage repair in other tissue types, yet a possible role for SIRT6 in male obesity and subfertility has not been investigated previously. To assess SIRT6 levels and activity in the testes, male mice (n = 12 per diet) were fed either a control diet (CD; 6% fat) or a high-fat diet (HFD; 21% fat) for 16 weeks before the collection of testes and spermatozoa. SIRT6 protein was localised to the nucleus of transitional spermatids and the acrosome of mature spermatozoa, with levels significantly decreased in HFD-fed male mice (P < 0.05). This decrease in SIRT6 protein was associated with transitional spermatids having increased levels of acetylated H3K9 in the nucleus (P < 0.01) and increased DNA damage (P < 0.001). We propose a role for SIRT6 in spermiogenesis and potentially protamination processes, which are known to be compromised by male obesity.

Knockout of nephron ATP6AP2 impairs proximal tubule function and prevents high fat diet induced obesity in male mice

Endocrinology ◽  
2021 ◽  
Author(s):  
Silas A Culver ◽  
Safia Akhtar ◽  
Callie Rountree-Jablin ◽  
Susanna R Keller ◽  
Helen P Cathro ◽  
...  
Keyword(s):  
Body Weight ◽  
Proximal Tubule ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Caloric Intake ◽  
Normal Diet ◽  
Male Mice ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Urinary Glucose

Abstract ATP6AP2 expression is increased in the nephron during high fat diet (HFD) and its knockout (ATP6AP2 KO) reduces body weight (WT) in mice. We evaluated the contribution of ATP6AP2 to urinary glucose (UG) and albumin (Ualb) handling during HFD. We hypothesized that nephron ATP6AP2 KO increases UG and Ualb and minimizes HFD-induced obesity. Eight-week old male C57BL/6J mice with inducible nephron specific ATP6AP2 KO and non-induced controls (C) were fed either normal diet (ND, 12% kcal fat) or HFD (45% kcal fat) for 6 months. ATP6AP2 KO mice on ND had 20% (p&lt;0.01) lower WT compared to C. HFD fed mice had 41% (p&lt;0.05) greater WT than ND fed C. In contrast, ATP6AP2 KO abrogated the increase in WT induced by HFD by 40% (p&lt;0.05). Mice on HFD had less caloric intake compared to ND controls (p&lt;0.01). There were no significant differences in metabolic rate between all groups. UG and Ualb was significantly increased in ATP6AP2 KO mice on both ND and HFD. ATP6AP2 KO showed greater levels of proximal tubule apoptosis and histologic evidence of proximal tubule injury. In conclusion, our results demonstrate that nephron specific ATP6AP2 KO is associated with glucosuria and albuminuria, most likely secondary to renal proximal tubule injury and/or dysfunction. Urinary loss of nutrients may have contributed to the reduced WT of knockout mice on ND and lack of WT gain in response to HFD. Future investigation should elucidate the mechanisms by which loss of renal ATP6AP2 causes proximal tubule injury and dysfunction.

scholarly journals Metabolic dysfunction in female mice with disruption of 5α-reductase 1

2017 ◽  
Vol 232 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Dawn E W Livingstone ◽  
Emma M Di Rollo ◽  
Tracy C-S Mak ◽  
Karen Sooy ◽  
Brian R Walker ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Stress Responses ◽  
High Fat Diet ◽  
Metabolic Dysfunction ◽  
Male Mice ◽  
High Fat ◽  
Female Mice ◽  
Normal Chow ◽  
Transcript Profiles

5α-Reductases irreversibly catalyse A-ring reduction of pregnene steroids, including glucocorticoids and androgens. Genetic disruption of 5α-reductase 1 in male mice impairs glucocorticoid clearance and predisposes to glucose intolerance and hepatic steatosis upon metabolic challenge. However, it is unclear whether this is driven by changes in androgen and/or glucocorticoid action. Female mice with transgenic disruption of 5α-reductase 1 (5αR1-KO) were studied, representing a ‘low androgen’ state. Glucocorticoid clearance and stress responses were studied in mice aged 6 months. Metabolism was assessed in mice on normal chow (aged 6 and 12 m) and also in a separate cohort following 1-month high-fat diet (aged 3 m). Female 5αR1-KO mice had adrenal suppression (44% lower AUC corticosterone after stress), and upon corticosterone infusion, accumulated hepatic glucocorticoids (~27% increased corticosterone). Female 5αR1-KO mice aged 6 m fed normal chow demonstrated insulin resistance (~35% increased area under curve (AUC) for insulin upon glucose tolerance testing) and hepatic steatosis (~33% increased hepatic triglycerides) compared with controls. This progressed to obesity (~12% increased body weight) and sustained insulin resistance (~38% increased AUC insulin) by age 12 m. Hepatic transcript profiles supported impaired lipid β-oxidation and increased triglyceride storage. Female 5αR1-KO mice were also predisposed to develop high-fat diet-induced insulin resistance. Exaggerated predisposition to metabolic disorders in female mice, compared with that seen in male mice, after disruption of 5αR1 suggests phenotypic changes may be underpinned by altered metabolism of glucocorticoids rather than androgens.

Sar1b transgenic male mice are more susceptible to high-fat diet-induced obesity, insulin insensitivity and intestinal chylomicron overproduction

2014 ◽  
Vol 25 (5) ◽  
pp. 540-548 ◽  
Author(s):  
Emile Levy ◽  
Schohraya Spahis ◽  
Carole Garofalo ◽  
Valérie Marcil ◽  
Alain Montoudis ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Male Mice ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Transgenic Male ◽  
Insulin Insensitivity

scholarly journals Effects of Curcumin in a Mouse Model of Very High Fat Diet-Induced Obesity

Biomolecules ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1368
Author(s):  
Iurii Koboziev ◽  
Shane Scoggin ◽  
Xiaoxia Gong ◽  
Parvin Mirzaei ◽  
Masoud Zabet-Moghaddam ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Protective Effects ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Dietary Interventions ◽  
Experimental Conditions ◽  
White Adipocyte ◽  
Diet Induced Obesity ◽  
Invaluable Tool ◽  
Very High

Worldwide rates of Western-diet-induced obesity epidemics are growing dramatically. Being linked with numerous comorbidities and complications, including cardiovascular disease, type 2 diabetes, cancer, chronic inflammation, and osteoarthritis (OA), obesity represents one of the most threatening challenges for modern healthcare. Mouse models are an invaluable tool for investigating the effects of diets and their bioactive components against high fat diet (HFD)-induced obesity and its comorbidities. During recent years, very high fat diets (VHFDs), providing 58–60% kcal fat, have become a popular alternative to more traditional HFDs, providing 40–45% total kcal fat, due to the faster induction of obesity and stronger metabolic responses. This project aims to investigate if the 60% fat VHFD is suitable to evaluate the protective effects of curcumin in diet-induced obesity and osteoarthritis. B6 male mice, prone to diet-induced metabolic dysfunction, were supplemented with VHFD without or with curcumin for 13 weeks. Under these experimental conditions, feeding mice a VHFD for 13 weeks did not result in expected robust manifestations of the targeted pathophysiologic conditions. Supplementing the diet with curcumin, in turn, protected the animals against obesity without significant changes in white adipocyte size, glucose clearance, and knee cartilage integrity. Additional research is needed to optimize diet composition, curcumin dosage, and duration of dietary interventions to establish the VHFD-induced obesity for evaluating the effects of curcumin on metabolic dysfunctions related to obesity and osteoarthritis.

scholarly journals Specific knockout of p85α in brown adipose tissue induces resistance to high-fat diet–induced obesity and its metabolic complications in male mice

2020 ◽  
Vol 31 ◽  
pp. 1-13 ◽  
Author(s):  
Almudena Gomez-Hernandez ◽  
Andrea R. Lopez-Pastor ◽  
Carlota Rubio-Longas ◽  
Patrik Majewski ◽  
Nuria Beneit ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Male Mice ◽  
High Fat ◽  
Metabolic Complications ◽  
Diet Induced Obesity ◽  
Brown Adipose

Glutaredoxin1 knockout promotes high-fat diet-induced obesity in male mice but not in female ones

2021 ◽  
Author(s):  
Xiao yu Zou ◽  
Muhammad Ijaz Ahmad ◽  
Di Zhao ◽  
Min Zhang ◽  
Chunbao Li
Keyword(s):  
High Fat Diet ◽  
Calorie Intake ◽  
Male Mice ◽  
High Fat ◽  
Male And Female ◽  
Female Mice ◽  
Diet Induced Obesity

This study aims to explore how high-fat diet and glutaredoxin1 (Glrx1) deficiency affect the development of obesity in male and female mice. High-fat diet induced great differences in calorie intake...

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