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American Journal of  Medical 
Science and Innovation (AJMSI) 

Effects of  Obesity in Male Fertility in Khartoum State
Khadeeja Yahya Othman Idrees1*, Roaa Mohamed Ahmed Elhaj2

Volume 3 Issue 2, Year 2024
ISSN: 2836-8509 (Online)

DOI: https://doi.org/10.54536/ajmsi.v3i2.3124
https://journals.e-palli.com/home/index.php/ajmsi

Article Information ABSTRACT

Received: September 05, 2024 

Accepted: October 02, 2024 

Published: October 05, 2024

Obesity is a severe medical condition causing health issues and reducing life expectancy, 
affecting 400 million adults and 1.6 million overweight individuals, is a severe medical 
condition affecting fertility, with extreme obesity causing fertility issues. This study aimed 
to investigate the effect of  obesity on male fertility in Khartoum state; it is a cross-sectional 
facility-based study studying All males of  Infertile couples who come to the infertility 
clinic. The study discussed patient demographics, past medical and surgical history, and 
self-reported male sexual dysfunction in addition to the factors that affect male infertility, 
Body Mass Index (BMI), and spermatic parameters (motility, morphology, concentration) by 
seminal analysis. The statistical package SPSS 23.0 was used for analysis. The study revealed 
that 40 men (20.5) were of  age <30 years old, 57 men (29.9%) of  age 30 – 40 years old, and 98 
men (50.3%) were of  age >40 years old. “One hundred five men (53.8%) were from North 
Sudan”, “58 men (29.7%) were from Eastern Sudan,30 men (15.35%) were from Western 
Sudan overweight, and 2 men (1.15%) were from Southern Sedan, 56 men (28.7%) have 
BMI <25,81(41.5%) had BMI 25 -30 and 58(29.8%) have BMI of  >30, 110 men (56.4%) 
have normal sperm counts and 85 (43.6) have abnormal sperm counts, 105 men (53.8%) 
have normal sperm morphology”. In contrast, 90 (46.2) have abnormal morphology. Eighty-
eight men (45.1%) have progressive motility, while 107 men (54.9%) have impaired motility. 
Fifty-six men (28.8%) of  participants have erectile dysfunction, while 139 (71.2%) have not. 
It concluded that increasing the age of  the male partner increases the risk of  infertility, and 
ethnicity has an unclear effect on infertility and still needs further studies to prove it. Obesity 
rates are increasing among men in Khartoum, impacting seminal parameters like motility and 
erectile dysfunction, as highlighted in a study.

Keywords
Body Mass Index, Male 
Infertility, Obesity, Reproduction, 
Research

1 King fahad hospital, Albaha, Saudi Arabia
2 Shagra hospital, Alriyadh, Saudi Arabia
* Corresponding author’s e-mail: khadeejaosman2@gmail.com

INTRODUCTION
Obesity is a severe medical condition characterized by 
the deposition of  excess body fat, which might adversely 
affect health and reduce life expectancy. A person could 
be classified as overweight if  his/her BMI is 25–30 kg/
m2, and obese if  BMI exceeds 30 kg/m2 (Bullen et al., 
2015).
Obesity is a global health issue with an epidemic 
proportion, with 400 million adults obese and 1.6 million 
overweight, accounting for 7.5% of  the disease burden 
(Palmer et al., 2012). It is associated with hormonal 
disturbance which negatively impact fertility, with women 
experiencing fertility in extreme obesity and weight loss, 
but this association is poorly characterized in males 
(Hammoud et al., 2008; Rufus et al., 2018).
Obesity in women leads to unproductive ovulation, 
decreased conception rates, and increased risk of  
miscarriage, while weight loss in ovulatory women 
improves fertility and conception rates. Obesity in male 
patients is linked to increased infertility, highlighting the 
need for increased clinician awareness and the increasing 
use of  Artificial Reproductive Technologies, particularly 
Intra-Cytoplasmic Sperm Injection (ICSI) (Barbagallo et 
al., 2021; Bullen et al., 2015).
Total body fat, intra-abdominal fat, and subcutaneous 
fat are all associated with low levels of  free and total 
testosterone in men, and most obese men looking for 

infertility treatment present with a decreased testosterone 
/ estrogen ratio (Carrageta et al., 2019). This is due to 
over activity of  the aromatase cytochrome P450 enzyme, 
which is expressed at high levels in white adipose tissue 
and is responsible for a key step in the biosynthesis of  
estrogens (Li et al., 2015; Steiner & Berry, 2022).
High levels of  estrogens in obese males result from 
the increased conversion of  androgens into estrogens 
owing to the high bioavailability of  these aromatase 
enzymes. Dysregulated levels of  sex hormones can 
cause great changes in both spermatogenesis and other 
aspects of  male reproduction. This observation indicates 
that estrogens might have a part in regulating the 
Hypothalamic Pituitary Gonadal (HPG) axis, suggesting 
that any amount of  excess estrogen could be detrimental 
(Chimento et al., 2014).
Resistin is another adipose tissue specific factor, which is 
reported to induce insulin resistance (Steppan & Lazar, 
2002). Hyperinsulinemia, which often occurs in obese 
men, has an inhibitory effect on normal spermatogenesis 
and can be linked to decreased male fertility in a group of  
diabetic men, semen parameters (concentration, motility 
and morphology) did not differ from the control group, 
but the amount of  nuclear and mitochondrial DNA 
damage in the sperm was significantly higher (Maresch et 
al., 2018; Oghbaei et al., 2021). 
The sperm DNA damage can impair male fertility 



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and reproductive health (Panner Selvam et al., 2021), 
in addition to inducing sperm DNA damage, insulin 
levels also have been shown to influence the levels of  
sex hormone binding globulin (sHBG), a glycoprotein 
that binds to sex hormones, specifically testosterone 
and estradiol, thereby inhibiting their biologic activity as 
carrier (Qu & Donnelly, 2020; Winters et al., 2014).
Obesity can lead to altered sperm production and 
parameters due to increased gonadal heat, which is a side 
effect of  increased scrotal adiposity (Chaudhuri et al., 
2022; Liu & Ding, 2017). The process of  spermatogenesis 
is highly sensitive to heat, with optimal temperature 
ranging between 34–35°C in humans. Increased testicular 
heat is associated with reduced sperm motility, increased 
sperm DNA damage and increased sperm oxidative stress 
(Hoang-Thi et al., 2022). 
Obesity and its causative agents, such as insulin resistance 
and dyslipidemia, are linked to increased oxidative stress, 
resulting in impaired sperm DNA damage and oxidative 
stress in obese patients (Leisegang, 2022; Manna & Jain, 
2015). This association is most likely the result of  the 
higher than usual metabolic rates required to maintain 
normal biological processes and an increased level of  
stress in the local testicular environment, both of  which 
naturally produce Reactive Oxygen Species (ROS). ROS 
is an independent marker of  male factor infertility and 
can lead to DNA damage, deformity and damaged plasma 
membrane integrity in sperm (Alahmar, 2019; Hosen et 
al., 2015).
Excess body weight can impair the feedback regulation 
of  the HPG axis, and all of  the factors above might 
contribute to, or be a result of, this dysregulation, which 
can contribute to apparent semen quality abnormalities. 
Obese, infertile men exhibit endocrine changes that are 
not observed in men with either obesity or infertility 
alone (Craig et al., 2017; Katib, 2015). This defective 
response to hormonal changes might be explained by 
partial or complete dysregulation of  the HPG axis (Dutta 
et al., 2019; Mintziori et al., 2020).
Because obesity can result from an unfavorable genotype 
and because obesity can cause infertility, a genetic link 
between these two factors might explain this discrepancy. 
Patients with Klinefelter, Prader–Willi or Laurence–
moon–Bardet–Biedel syndromes all display, to varying 
degrees, both obesity and infertility (Chaudhuri et al., 
2022; Krausz et al., 2022; Tornese et al., 2020). In addition, 
men who are both infertile and obese show significantly 
lower testosterone levels than obese fertile men (Stokes 
et al., 2015).
Due to difficulties in interpreting data from human studies, 
rodent models of  male obesity have now been established 
to assess the impact of  male obesity on sperm function, 
however it is necessary to be aware of  the differences 
between species. These studies have demonstrated that 
males fed a high fat diet to induce obesity had reduced 
sperm motility and a decrease in percentage of  sperm 
with normal morphology (Mu et al., 2017).
Numerous human studies as well as animal study have 

determined that a relationship between obesity and 
reduced sperm DNA integrity exists, despite the use 
of  a variety of  different methodologies to measure 
sperm DNA integrity (TUNEL, COMET, SCSA, etc.) 
(Evenson, 2017; Javed et al., 2019; Román Montañana, 
2020). Only two studies, one human and one rodent have 
directly linked levels of  sperm oxidative stress with male 
BMI. Both studies concluded that a positive association 
between increasing BMI and increased sperm oxidative 
stress exists (Jing et al., 2023).
Another Retrospective study done in a Referral fertility 
center in UK 2008 revealed that “the incidence of  
oligozoospermia increased with increasing BMI: normal 
weight ¼ 5.32%, overweight ¼ 9.52%, and obese ¼ 
15.62%. The prevalence of  a low progressively motile 
sperm count was also greater with increasing BMI: 
normal weight ¼ 4.52%, overweight ¼ 8.93%, and obese 
¼ 13.28%. The incidence of  erectile dysfunction did not 
vary across BMI categories when corrected for potential 
contributing factors (9).
The study aimed to investigate the impact of  male 
obesity on spermatic parameters (morphology, motility 
and concentration), erectile dysfunction rates, and 
the relationship between personal characteristics and 
infertility.

MATERIALS AND METHODS
Study Design & Area
The present research study is a Cross-sectional facility-
based study, conducted at Bnoon Infertility Center and 
Saad Abu Alaa Infertility Center in Khartoum state. 
Saad Abu Ellaa Infertility Center, the first governmental 
specialized center in Sudan, is managed by Khartoum 
University and has highly qualified staff. It offers IVF at 
the lowest possible cost, with an average of  1000-1200 
patients per year. Bnoon Infertility Center, a private 
specialized center in Khartoum, Sudan, is well-known 
with an average of  1500-2000 patients seen annually, 
representing the private sector.

Study Duration
The study was conducted for approximately six months 
spanning from January 2018 to June 2018. 
Study Population  
All male individuals from infertile couples seeking 
treatment at the infertility center. 

Inclusion Criteria 
Males from couples who have been married for at least 

one year and do not have any siblings. 
• Males from couples who have been married for at 

least one year and do not have any siblings.  

Exclusion Criteria 
• Males from couples who have been married for less 

than one year. 
• Males who do not engage in regular intercourse due 

to the reasons such as husbands travelling abroad.



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• Males who decline to sign the consent form.
• Males with co-existing conditions such as diabetes 

mellitus, hypertension, or a history of  undescended testis. 

Sample Size
The sample size will be calculated by using the given 
formula:
 N=Z2 PQ/D2
Where,
N= Sample Size
Z= Standard Deviation taken as 1.96 at a 95% confidence 
interval
P= Estimated Prevalence, assumed as 0.5 or 50%
Q= 1-P, also 0.5 in this case  
D= Total Coverage initially set at a 385 patients.

Independent Variables
Age of  individuals measured in years
Ethnicity: The cultural or ancestral background of  
individuals, categorized in specific ethnic groups. 
Body Mass Index (BMI): A measurement of  body fats 
based on height and weight used to access health status 
related to weight. 

Dependent Variables 
The dependent variables include oligospermia, 
azoospermia, abnormal sperm morphology, abnormal 
sperm motility, and erectile dysfunction. 

Data Collection
Confidential questionnaires were used to gather data 

on patient demographics, medical history, male sexual 
dysfunction, factors influencing infertility, BMI, and 
seminal analysis parameters such as motility, morphology, 
and concentration. The participants filled out the 
questionnaire in a highly confidential manner. 

Data Analysis
The means were reported as Mean ± Standard error. 
The Chi-Square test for trend was utilized to compare 
frequencies and logistic regression analysis was applied 
and deemed suitable. Statistical analysis was conducted 
by using the SPSS 23.0 software package (SPSS, Chicago, 
IL). 

Ethical Considerations 
Ethical approval was obtained from the infertility centers 
before the intervention, including approval from the 
ethical committee. All men included in the study received 
written consent, with the study purpose explained to 
them. The questionnaire was filled out confidentially and 
voluntarily by the nominated participants. Patients had 
the right to decide whether to participate in the study or 
not. 

RESULTS AND DISCUSSION
Results
Selected Participants
In the present study, 40 men (20.5%) were under the age 
of  30, and 57mean (29.9%) were between the ages of  30 
and 40, while 98 men (50.3%) were over the age of  40. 

Table 1: Frequency of  Age Groups Among Participants 
Age group No. of  participant Percentage of  participants
<30 years old 40 20.5%
30 – 40 years old 57 29.2%
>40 years old 98 50.3%

Figure 1: Frequency of  Ethnic Groups Among Participants

Of  this study 105 men (53.8%) were from North Sudan, 
58 men (29.7%) were from Eastern Sudan, 30 men 
(15.35%) are from Western Sudan overweight and 2 
men (1.15%) were from Southern Sudan. of  the study, 
110 men (56.4%) have normal sperm counts and 85 

(43.6) have abnormal sperm counts, 105 men (53.8%) 
have normal sperm morphology while 90 (46.2) have 
abnormal morphology. 88 men (45.1%) have progressive 
motility while 107 men (54.9%) have impaired motility.



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Discussion 
In the present research study, it was observed that the 
majority of  participants, out of  a total of  195 men, were 
aged over 40 years, accounting for 50.3% of  all participants. 
This was followed by individuals aged between 30 and 40 
years, representing 29.95%, while those below 30 years 
old constituted the smallest proportion at 20.5% of  all 
participants (Harris et al., 2011). 
This finding is corroborated by a French study 
that investigated 901 cycles of  intrauterine artificial 
insemination. The study identified the age of  the male 
partner as the most influential factor affecting the 
likelihood of  pregnancy. After six cycles, men aged 35 
years or older exhibited a fertility rate of  25%, contrasting 
with a fertility rate of  52% among men under 35 years 
old, reflecting 52%reduction in fertility rate.
The majority of  participants, compromising 53.8%, hailed 
from North Sudan with Eastern Sudan contributing 
29.7% of  the participants. Western Sudan accounted 
for 15.35% of  the sample, while Southern Sudanese 
participants constituted the smallest group at 1.15%. 
Despite the evident disparity in participant distribution 
across ethnic groups, statistical analysis revealed no 
significant association between BMI, infertility and ethnic 
groups, with respective p-values of  0.4 and 0.7. 
Among the participants, 81% had a BMI ranging from 
25 to 30, with 58% having a BMI exceeding 30 kg/m2, 
and only 28.7% having a BMI below 25 kg/m2. Figure 2 
provided a visual depiction of  these distributions. These 
results are consisted with prior research indicating a 
troubling rise in male obesity among men of  reproductive 
age, nearly tripling over the past three decades, coinciding 
with a global increase in male fertility rates. Emerging 
evidence suggests that male obesity adversely effects 

Figure 2: Frequency of  Body Mass Index Among Participants 

Figure 4: Frequency of  Participants With Erectile 
Dysfunction 

Figure 3: Multiple Liner Regression for BMI & Seminal 
Parameters

Table 2: Frequencies of  Seminal Parameters Among Participants 
Seminal analysis No. of  participant 

Normal Abnormal
Sperms count 110 85
Sperms morphology 105 90
Sperms progressive motility 88 107



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reproductive potential, impacting not only sperm quality 
but also inducing structural and molecular changes in 
germs cells within the testes and ultimately in mature 
sperm. Direct associations have been found between male 
BMI and DNA fragmentation in sperm, with higher BMI 
levels correlating with increased sperm fragmentation 
(Harris et al., 2011). 
In April 2016, a study conducted in the UK found a 
significant decrease in sperm quality among men with a 
BMI over 25, with even more severe effects observed in 
those with a BMI over 30. This decline in sperm quality, 
particularly characterized by fragmented sperm DNA, 
is associated with an increased risk of  early miscarriage. 
The silent challenge of  infertility among obese men 
underscores the importance of  addressing this health 
issue, as highlighted in the present research. These findings 
emphasize the need for attention from policymakers and 
the media to raise awareness and promote inventions in 
this area (G Alves et al., 2016; Hammoud et al., 2008). 
Although it was found that 56.4% of  participants had 
normal sperm counts, and 53% exhibited normal sperm 
morphology. However, only 45.1% showed normal 
progressive motility, as presented in Table 3. A study 
conducted in the USA in 2008 at a referral clinic revealed 
that the incidence of  oligozoospermia increased with 
higher BMI categories: 5.32% among normal weight 
individuals, 9.52% among overweight individuals, and 
15.62% among obese individuals. Similarly, the prevalence 
of  a low progressively motile sperm counts also increased 
with increasing BMI: 4.52% among normal weight 
individuals, 8.93% among overweight individuals, and 
13.28% among obese individuals (Hammoud et al., 2008). 
Recent population based studied conducted over the past 
5-10 years have revealed a higher prevalence of  abnormal 
semen parameters among overweight and obese men, 
suggesting a potential association with subfertility in 
couples where the male partner is obese (Du Plessis et 
al., 2010).
Additionally, it was found that obesity impacts genetic 
and epigenetic mechanisms, inhibiting chromatin 
condensation, increasing DNA fragmentation, causing 
apoptosis and alteration in spermatozoa, disrupting 
sperm morphology and functions, and potentially causing 
inherited epigenetic alterations in offspring (Dutta et al., 
2019; Leisegang et al., 2021).
Leptin, a hormone produced by adipose tissue, increases 
with body fat, affecting reproductive function. Obese 
men may not be sensitive to increased leptin production, 
leading to functional leptin resistance. While Kisspeptin 
neurons mediate leptin’s effects on the reproductive 
system, potentially causing increased infertility 
(Ghaderpour et al., 2022). 
Furthermore, through, endocrinopathy obesity effects 
male fertility, aromatization, erectile dysfunction, 
psychological effects, sleep apnea, leptin, oxygen free 
radicals, and epididymitis. Treatment includes weight 
reduction, aromatase inhibitors, gonadotropins, 
phosphodiesterase inhibitors, and insulin-sensitizing 

agents (El Salam, 2018). 
The present study assessed the impact of  obesity on 
epididymal and germinal epithelia revealed significant 
finding. Circulating leptin and estradiol levels exhibited 
a notable increase, while testosterone levels declined. 
Additionally, there was an observed increase in 
lipid peroxidation in the epididymis and a reduction 
in spermatobioscopic parameters. Morphological 
differences were noted in the heads of  the epididymis in 
obese rats, although no significant variance was observed 
in the testes between the two groups (Vigueras-Villaseñor 
et al., 2011). These results provide clear evidence of  an 
adverse effect on sperm in obese rats, particularly evident 
in the epididymis. 
However, all studies consistently demonstrated a clear 
association between obesity and male fertility, this 
particular study was found no significant association in 
terms of  reduced progressive sperm motility. The linear 
regression analysis yielded a non-significant p-value of  
0.3, as illustrated in Figure 3 of  the histogram. This lack 
of  significance can be attributed mainly to the suboptimal 
sample size used in the study.
Only 25.2% of  the participants experienced erectile 
dysfunction. An Italian study published in The Journal 
of  Sexual Medicine, examined 2,435 Italian male patients 
who sought outpatient treatment for sexual dysfunction 
from 2001 to 2007. The participants were categorized 
as follows: 41.5% were normal weight, 42.4% were 
overweight, 12.1% were obese and 4% were severely 
obese. The average age of  the participants was 52 years 
old. Patients underwent laboratory blood tests and a 
penile Doppler ultrasound to assess penile blood flow. 
Additionally, they were interviewed regarding their erectile 
dysfunction and completed a mental health assessment 
(Esposito et al., 2008). 

LIMITATIONS
• The study’s small sample size hindered the detection 

of  significant differences, particularly regarding the 
impact of  obesity on infertility.

• The study’s generalizability was limited, because it 
purely focused on men in Khartoum, requiring a more 
diverse sample to better understand ethnicity’s impact on 
infertility.

• The use of  self-reported data, particularly in erectile 
dysfunction and lifestyle factors like obesity, can introduce 
potential bias and inaccuracies.

CONCLUSION
The study concluded various factors related to male 
fertility, including age, ethnicity and obesity. It found 
that advancing age of  the male partner increases the 
risk of  infertility, while the impact of  ethnicity on 
infertility remains uncertain and requires further research. 
Additionally, the study noted a rising trends of  obesity 
among men in Khartoum and highlighted its detrimental 
effects on seminal parameters, particularly sperm motility. 
Moreover, obesity was linked to an increased risk of  



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erectile dysfunction. However, the study failed to identify 
a statistically difference in infertility related to obesity, 
possibly due to the small sample size. 

RECOMMENDATIONS
• Large-scale studies with a diverse participant pool 

can improve the statistical power and generalizability of  
findings on obesity’s impact on infertility.

• Longitudinal research designs can help track changes 
over time and establish causal relationships between 
advancing age, obesity, and infertility outcomes.

• Biomarkers, including objective measures like obesity, 
reproductive hormones, and semen quality, can offer 
more reliable data and reduce reliance on self-reported 
information.

• Collaborating with multiple research centers across 
different regions can expand the study’s scope and 
better understand infertility risk factors among diverse 
populations.
 
REFERENCES
Abd El Salam, M. A. (2018). Obesity, an enemy of  male 

fertility: a mini review. Oman medical journal, 33(1), 3. 
Alahmar, A. T. (2019). Role of  oxidative stress in 

male infertility: an updated review. Journal of  human 
reproductive sciences, 12(1), 4-18. 

Barbagallo, F., Condorelli, R. A., Mongioì, L. M., 
Cannarella, R., Cimino, L., Magagnini, M. C., Crafa, 
A., La Vignera, S., & Calogero, A. E. (2021). Molecular 
mechanisms underlying the relationship between 
obesity and male infertility. Metabolites, 11(12), 840. 

Bullen, V., Judge, S., & Bullen, V. (2015). The impact of  
obesity on male fertility. British Journal of  Obesity, 1(3), 
99-107. 

Carrageta, D. F., Oliveira, P. F., Alves, M. G., & Monteiro, 
M. P. (2019). Obesity and male hypogonadism: Tales 
of  a vicious cycle. Obesity Reviews, 20(8), 1148-1158. 

Chaudhuri, G. R., Das, A., Kesh, S. B., Bhattacharya, 
K., Dutta, S., Sengupta, P., & Syamal, A. K. (2022). 
Obesity and male infertility: multifaceted reproductive 
disruption. Middle East Fertility Society Journal, 27(1), 8. 

Chimento, A., Sirianni, R., Casaburi, I., & Pezzi, V. (2014). 
Role of  estrogen receptors and G protein-coupled 
estrogen receptor in regulation of  hypothalamus–
pituitary–testis axis and spermatogenesis. Frontiers in 
Endocrinology, 5, 78379. 

Craig, J. R., Jenkins, T. G., Carrell, D. T., & Hotaling, J. 
M. (2017). Obesity, male infertility, and the sperm 
epigenome. Fertility and sterility, 107(4), 848-859. 

Du Plessis, S. S., Cabler, S., McAlister, D. A., Sabanegh, 
E., & Agarwal, A. (2010). The effect of  obesity on 
sperm disorders and male infertility. Nature Reviews 
Urology, 7(3), 153-161. 

Dutta, S., Biswas, A., & Sengupta, P. (2019). Obesity, 
endocrine disruption and male infertility. Asian Pacific 
Journal of  Reproduction, 8(5), 195-202. 

Esposito, K., Giugliano, F., Ciotola, M., De Sio, M., 
D’armiento, M., & Giugliano, D. (2008). Obesity 

and sexual dysfunction, male and female. International 
journal of  impotence research, 20(4), 358-365. 

Evenson, D. P. (2017). Evaluation of  sperm chromatin 
structure and DNA strand breaks is an important 
part of  clinical male fertility assessment. Translational 
andrology and urology, 6(Suppl 4), S495. 

G Alves, M., T Jesus, T., Sousa, M., Goldberg, E., M Silva, 
B., & F Oliveira, P. (2016). Male fertility and obesity: 
are ghrelin, leptin and glucagon-like peptide-1 
pharmacologically relevant? Current Pharmaceutical 
Design, 22(7), 783-791. 

Ghaderpour, S., Ghiasi, R., Heydari, H., & Keyhanmanesh, 
R. (2022). The relation between obesity, kisspeptin, 
leptin, and male fertility. Hormone Molecular Biology and 
Clinical Investigation, 43(2), 235-247. 

Hammoud, A. O., Wilde, N., Gibson, M., Parks, A., 
Carrell, D. T., & Meikle, A. W. (2008). Male obesity 
and alteration in sperm parameters. Fertility and sterility, 
90(6), 2222-2225. 

Harris, I. D., Fronczak, C., Roth, L., & Meacham, R. B. 
(2011). Fertility and the aging male. Reviews in urology, 
13(4), e184. 

Hoang-Thi, A.-P., Dang-Thi, A.-T., Phan-Van, S., 
Nguyen-Ba, T., Truong-Thi, P.-L., Le-Minh, T., 
Nguyen-Vu, Q.-H., & Nguyen-Thanh, T. (2022). 
The impact of  high ambient temperature on human 
sperm parameters: A meta-analysis. Iranian Journal of  
Public Health, 51(4), 710. 

Hosen, M. B., Islam, M. R., Begum, F., Kabir, Y., & Howlader, 
M. Z. H. (2015). Oxidative stress induced sperm DNA 
damage, a possible reason for male infertility. Iranian 
journal of  reproductive medicine, 13(9), 525. 

Javed, A., Talkad, M. S., & Ramaiah, M. K. (2019). 
Evaluation of  sperm DNA fragmentation using 
multiple methods: a comparison of  their predictive 
power for male infertility. Clinical and experimental 
reproductive medicine, 46(1), 14. 

Jing, J., Peng, Y., Fan, W., Han, S., Peng, Q., Xue, C., 
Qin, X., Liu, Y., & Ding, Z. (2023). Obesity induced 
oxidative stress and mitochondrial dysfunction 
negatively affect sperm quality. FEBS Open bio, 13(4), 
763-778. 

Katib, A. (2015). Mechanisms linking obesity to male 
infertility. Central European journal of  urology, 68(1), 79. 

Krausz, C., Rosta, V., Swerdloff, R. S., & Wang, C. (2022). 
Genetics of  male infertility. Emery and rimoin’s principles 
and practice of  medical genetics and genomics, 121-147. 

Leisegang, K. (2022). Oxidative stress in men with obesity, 
metabolic syndrome and type 2 diabetes mellitus: 
Mechanisms and management of  reproductive 
dysfunction. In Oxidative Stress and Toxicity in 
Reproductive Biology and Medicine: A Comprehensive Update 
on Male Infertility-Volume One (pp. 237-256). Springer. 

Leisegang, K., Sengupta, P., Agarwal, A., & Henkel, R. 
(2021). Obesity and male infertility: Mechanisms and 
management. Andrologia, 53(1), e13617. 

Li, J., Papadopoulos, V., & Vihma, V. (2015). Steroid 
biosynthesis in adipose tissue. Steroids, 103, 89-104. 



Pa
ge

 
90

https://journals.e-palli.com/home/index.php/ajmsi

Am. J. Med. Sci. Innov. 3(2) 84-90, 2024

Liu, Y., & Ding, Z. (2017). Obesity, a serious etiologic 
factor for male subfertility in modern society. 
Reproduction, 154(4), R123-R131. 

Manna, P., & Jain, S. K. (2015). Obesity, oxidative stress, 
adipose tissue dysfunction, and the associated health 
risks: causes and therapeutic strategies. Metabolic 
syndrome and related disorders, 13(10), 423-444. 

Maresch, C. C., Stute, D. C., Alves, M. G., Oliveira, P. F., de 
Kretser, D. M., & Linn, T. (2018). Diabetes-induced 
hyperglycemia impairs male reproductive function: a 
systematic review. Human Reproduction Update, 24(1), 
86-105. 

Mintziori, G., Nigdelis, M. P., Mathew, H., Mousiolis, A., 
Goulis, D. G., & Mantzoros, C. S. (2020). The effect 
of  excess body fat on female and male reproduction. 
Metabolism, 107, 154193. 

Mu, Y., Yan, W.-j., Yin, T.-l., Zhang, Y., Li, J., & Yang, J. 
(2017). Diet-induced obesity impairs spermatogenesis: 
A potential role for autophagy. Scientific reports, 7(1), 
43475. 

Oghbaei, H., Fattahi, A., Hamidian, G., Sadigh-Eteghad, 
S., Ziaee, M., & Mahmoudi, J. (2021). A closer 
look at the role of  insulin for the regulation of  
male reproductive function. General and comparative 
endocrinology, 300, 113643. 

Palmer, N. O., Bakos, H. W., Fullston, T., & Lane, M. 
(2012). Impact of  obesity on male fertility, sperm 
function and molecular composition. Spermatogenesis, 
2(4), 253-263. 

Panner Selvam, M. K., Ambar, R. F., Agarwal, A., & 
Henkel, R. (2021). Etiologies of  sperm DNA damage 
and its impact on male infertility. Andrologia, 53(1), 
e13706. 

Qu, X., & Donnelly, R. (2020). Sex hormone-binding 
globulin (SHBG) as an early biomarker and therapeutic 
target in polycystic ovary syndrome. International 
journal of  molecular sciences, 21(21), 8191. 

Román Montañana, C. (2020). Assessment of  DNA structure 
and integrity in the human spermatozoon University of  
Birmingham]. 

Rufus, O., James, O., & Michael, A. (2018). Male obesity 
and semen quality: Any association? International 
Journal of  Reproductive Biomedicine, 16(4), 285. 

Steiner, B. M., & Berry, D. C. (2022). The regulation 
of  adipose tissue health by estrogens. Frontiers in 
Endocrinology, 13, 889923. 

Steppan, C. M., & Lazar, M. A. (2002). Resistin and 
obesity-associated insulin resistance. Trends in 
endocrinology & Metabolism, 13(1), 18-23. 

Stokes, V. J., Anderson, R. A., & George, J. T. (2015). How 
does obesity affect fertility in men–and what are the 
treatment options? Clinical Endocrinology, 82(5), 633-638. 

Tornese, G., Pellegrin, M. C., Barbi, E., & Ventura, A. 
(2020). Pediatric endocrinology through syndromes. 
European journal of  medical genetics, 63(1), 103614. 

Vigueras-Villaseñor, R. M., Rojas-Castañeda, J. C., 
Chávez-Saldaña, M., Gutiérrez-Pérez, O., García-
Cruz, M. E., Cuevas-Alpuche, O., Reyes-Romero, 
M. M., & Zambrano, E. (2011). Alterations in the 
spermatic function generated by obesity in rats. Acta 
histochemica, 113(2), 214-220. 

Winters, S. J., Gogineni, J., Karegar, M., Scoggins, C., 
Wunderlich, C. A., Baumgartner, R., & Ghooray, 
D. T. (2014). Sex hormone-binding globulin gene 
expression and insulin resistance. The Journal of  Clinical 
Endocrinology & Metabolism, 99(12), E2780-E2788. 


