Diet and exercise in an obese mouse fed a high-fat diet improve metabolic health and reverse perturbed sperm function

2012 ◽  
Vol 302 (7) ◽  
pp. E768-E780 ◽  
Author(s):  
Nicole O. Palmer ◽  
Hassan W. Bakos ◽  
Julie A. Owens ◽  
Brian P. Setchell ◽  
Michelle Lane
Keyword(s):  
Dna Damage ◽  
Sperm Motility ◽  
Serum Cholesterol ◽  
High Fat Diet ◽  
Sperm Function ◽  
High Fat ◽  
Exercise Interventions ◽  
Sperm Dna Damage ◽  
Sperm Dna ◽  
Diet And Exercise

Male obesity is associated with reduced sperm motility and morphology and increased sperm DNA damage and oxidative stress; however, the reversibility of these phenotypes has never been studied. Therefore, the aim of this study was to assess the reversibility of obesity and its associated sperm physiology and function in mice in response to weight loss through diet and exercise. C57BL6 male mice ( n = 40) were fed either a control diet (CD; 6% fat) or a high-fat diet (HFD; 21% fat) for 10 wk before allocation to either diet and/or swimming exercise interventions for 8 wk. Diet alone reduced adiposity (1.6-fold) and serum cholesterol levels (1.7-fold, P < 0.05), while exercise alone did not alter these, but exercise plus diet also improved glucose tolerance (1.3-fold, P < 0.05). Diet and/or exercise improved sperm motility (1.2-fold) and morphology (1.1-fold, P < 0.05), and reduced sperm DNA damage (1.5-fold), reactive oxygen species (1.1-fold), and mitochondrial membrane potential (1.2-fold, P < 0.05) and increased sperm binding (1.4-fold) ( P < 0.05). Sperm parameters were highly correlated with measures of glycemia, insulin action, and serum cholesterol (all P < 0.05) regardless of adiposity or intervention, suggesting a link between systemic metabolic status and sperm function. This is the first study to show that the abnormal sperm physiology resulting from obesity can be reversed through diet and exercise, even in the presence of ongoing obesity, suggesting that diet and lifestyle interventions could be a combined approach to target subfertility in overweight and obese men.

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.

147. PATERNAL OBESITY IMPAIRS SPERM FUNCTION AND SUBSEQUENT EMBRYO AND PREGNANCY OUTCOMES

2009 ◽  
Vol 21 (9) ◽  
pp. 65
Author(s):  
H. W. Bakos ◽  
M. Mitchell ◽  
B. P. Setchell ◽  
M. Lane
Keyword(s):  
Dna Damage ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Cell Number ◽  
Blastocyst Stage ◽  
Reproductive Age ◽  
Sperm Function ◽  
Blastocyst Development ◽  
Sperm Dna Damage ◽  
Sperm Dna

Despite the increased prevalence of obesity in males of reproductive age, the effects of male obesity on conception and pregnancy have been largely ignored. Hence, the aim of this study was to elucidate the effects of paternal Diet Induced Obesity (DIO) on sperm function, embryo development and pregnancy. Six week old C57BL/6 male mice (n=36) were allocated to either standard chow or a high fat diet (HFD). After eight weeks, mice were either sacrificed and spermatozoa assessed, for motility, reactive oxygen species (ROS) and DNA damage or mated and zygotes collected and cultured to the blastocyst stage. Blastocyst development, cell number and apoptosis were assessed, and fetal outcomes analyzed following embryo transfer. Differences between treatments were assessed using GLM. The percentage of motile spermatozoa was decreased (36% vs. 44%, p<0.05) in the HFD group compared to controls. Intracellular ROS were elevated (692units vs. 409units, p<0.01) in the HFD group compared to controls. Overall levels of sperm DNA damage were also increased (1.64% vs. 0.17%, p<0.05) in the HFD group. Blastocyst development was reduced when males were fed a HFD (64% vs. 84%, p<0.05). Similarly, blastocyst cell number (37.9±2.8 vs. 46.6±2.5, p<0.05), inner cell mass number (11.4±0.9 vs. 15.3±0.9, p<0.05) were reduced and apoptosis (12.8±1.9 vs. 6.6±0.6, p<0.05) increased in embryos sired by a male fed a HFD. Implantation (86.7% vs. 72.5%, p<0.05) and fetal development (38.7% vs. 22.5% p<0.05) were also significantly reduced when blastocysts came from a male fed a HFD. This is the first report providing comprehensive evidence that paternal DIO significantly impairs embryo quality and pregnancy rates. These effects may be related to the observed increase in oxidative stress and sperm DNA damage. These data provide compelling evidence that male obesity impacts on male fertility, embryos as well as pregnancy and therefore studies in human are warranted.

Altered bone metabolism after high fat diet and exercise: role of Wnt signaling and insulin resistance

2016 ◽  
Author(s):  
Ann-Kristin Picke ◽  
Lykke Sylow ◽  
Lisbeth L V Moller ◽  
Rasmus Kjobsted ◽  
Erik Richter ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Wnt Signaling ◽  
Bone Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
Diet And Exercise
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