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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 42  |  Issue : 3  |  Page : 103-111

Obestatin and l-carnitine as a defensive strategy against fertility disorders induced by obesity in male rats


1 Department of Physiology, Faculty of Medicine, Tanta University, Tanta, Egypt; Department of Physiology, Faculty of Medicine, University of Tabuk, Tabuk, Saudi Arabia
2 Department of Physiology, Faculty of Medicine, Tanta University, Tanta, Egypt; Department of Physiology, Faculty of Medicine, University of Tabuk, Tabuk; Department of Basic Dental and Medical Sciences, Faculty of Dentistry, Al-Qassim University, Buridah, Saudi Arabia

Date of Submission12-Jun-2014
Date of Acceptance20-Jul-2014
Date of Web Publication29-Oct-2014

Correspondence Address:
Mahmoud E Salama
MD, Department of Physiology, Faculty of Medicine, Tanta University, Tanta, Egypt

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DOI: 10.4103/1110-1415.143565

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  Abstract 

Aim
This study was designed to investigate the usage of obestatin (OB) and l-carnitine (LC) as a defensive strategy against fertility disorders induced by obesity in male rats.
Materials and methods
The study was carried out on 50 male Wistar rats, which were divided into five groups as follows: the control group, untreated obese rats, obese rats treated with OB, obese rats treated with LC, and obese rats treated with both OB and LC.
Results
The induction of obesity resulted in significant increase in body weight, plasma level of triglyceride, total cholesterol, low-density lipoprotein-cholesterol, and thiobarbituric acid reactive substance as compared with the control group. In addition, it produced significant lower activities of superoxide dismutase, catalase, and glutathione peroxidase antioxidant enzymes (GHP-Px) in testicular tissue. There was reduced plasma testosterone, follicle stimulating hormone, luteinizing hormone, and low-density lipoprotein-cholesterol and decreased sperm count and motility. OB significantly lowers body weight, plasma levels triglyceride, total cholesterol, low--density lipoprotein-cholesterol, and testicular thiobarbituric acid reactive substance level. These changes were coupled with significant increase in antioxidant enzymes activities in testicular tissue with significant increase in testosterone plasma level and sperm count and motility. This was accompanied by insignificant increase in plasma follicle stimulating hormone and luteinizing hormone levels. LC produced similar but better changes in all parameters except body weight. Moreover, the concomitant administration of both OB and LC to obese rats resulted in more improvement in all parameters than that were noticed in group III or IV.
Conclusion
The results of the study verified the possible combined use of OB and LC as a defensive strategy against fertility disorders induced by obesity. OB has the upper hand as anorexigenic agent, whereas LC is superior against obesity as a case of secondary hypogonadism.

Keywords: Fertility, l-carnitine, obesity, obestatin, oxidative stress, semen, testosterone


How to cite this article:
El-Damarawi MA, Salama ME. Obestatin and l-carnitine as a defensive strategy against fertility disorders induced by obesity in male rats. Tanta Med J 2014;42:103-11

How to cite this URL:
El-Damarawi MA, Salama ME. Obestatin and l-carnitine as a defensive strategy against fertility disorders induced by obesity in male rats. Tanta Med J [serial online] 2014 [cited 2017 Aug 23];42:103-11. Available from: http://www.tdj.eg.net/text.asp?2014/42/3/103/143565


  Introduction Top


Nowadays, obesity is considered as one of the major health problems all over the world whether in the developed or developing countries. It is a complex multifactorial disease that grows from the interaction between genotype and the environment, which involves the integration of social, behavioral, cultural, physiological, and metabolic factors [1]. According to the WHO, overweight and obesity are main risk factors for a number of chronic diseases including diabetes, dyslipidemia, hypertension, metabolic syndrome, cardiovascular diseases, cancer, and certain reproductive and metabolic disorders [2].

Obesity is assessed by evaluating BMI, waist circumference, body weight, and overall medical risks. In humans, obesity adversely affects male fertility by decreasing spermatogenesis and producing endocrinal abnormalities, sexual dysfunction, and oxidative stress [3],[4]. Furthermore, increased BMI causes poor semen quality, decreased sperm concentration, decreased normal motile sperm cells, and increased DNA fragmentation index [5].

Obesity causes an increase in estradiol production from testosterone, with subsequent decreased secretion of luteinizing hormone (LH) and follicle stimulating hormone (FSH). Consequently, obesity was considered to be one of the possible causes of secondary hyperestrogenic hypogonadism and associated infertility in many patients [6].

Obesity causes proinflammatory adipokines augmentation, which is responsible for the increase in testicular oxidative stress that leads fertility disorders [7].

Testosterone, the male hormone, elevates the metabolism and increases the release of fat from fat cells and inhibits its storage in the body.

Obesity is associated with low serum testosterone level. Testosterone and body fat content have bidirectional relationship, which means that excess body fat causes low serum testosterone level, and testosterone deficiency is one of the etiological factors of obesity [8].

The low testosterone level in obesity may be due to a problem at the level of the hypothalamus or pituitary to produce appropriate amounts of LH and FSH and/or decrease the response of the testes to these hormones [9]. Consequently, the sperm's quality may be affected and there may also be a low sperm count.

Obestatin (OB) is present in many sites including plasma, mucosa of the gastrointestinal tract, mammary glands, and interstitial cells of Leydig in the testis [10]. It is a hormone that shares mainly in the regulation of food intake. Treatment of rodents with OB suppresses food intake, inhibits jejunal contractions, and decreases body weight [11] . OB level was reported to decrease in obese individuals and there was an elevated ratio of circulating preprandial ghrelin to OB ratio in human obesity [12].

OB expression has been reported in the Leydig cells of testes [13]; however, the specific role of OB in the regulation of reproductive functions is still unknown.

Previous study showed that single intravenous injection of OB increased testosterone secretion in adult male rats. In addition, chronic infusion of OB during the pubertal stage significantly increased the testosterone level in the adult male rats [14],[15].

l-Carnitine (LC), which is derived from lysine and methionine, is essential for β-oxidation of long-chain fatty acids in mitochondria. LC exerts a substantial antioxidant action, thereby providing a protective effect against lipid peroxidation of phospholipid membranes and against oxidative stress [16],[17].

LC reduces serum levels of triglyceride (TG) and very-low-density lipoprotein-cholesterol (VLDL-C) and increases high-density lipoprotein-cholesterol (HDL-C) and albumin. In addition, some studies showed that oral LC reduces fat mass and increases muscle mass. All these effects may contribute to weight loss [18,19].

Low sperm counts have been linked to low LC levels in men. In contrast, LC supplements may increase sperm count and mobility in rats exposed to physical insults and in clinical trials conducted in men with idiopathic oligoasthenospermia [17],[20].

The aim of the present work was designated to study OB and LC as a defensive strategy against fertility disorders induced by obesity in male rats. We chose OB and LC as they are naturally occurring in our bodies. Their levels are decreased in obesity and increased after weight loss. Hence, we aimed to test whether their administration, especially together, can prevent the development of a group of fertility disorders induced by obesity.


  Materials and methods Top


Experimental animals

This study was performed on 50 male Wistar rats weighing 180-230 g. The handling of the animals was carried out in accordance with the ethical guidelines for investigations and approved by the Local Ethical Committee for the Care and Use of Laboratory Animals. The rats were housed in isolated animal cages and kept under a 12-h light-dark cycle at room temperature and humidity 70-75%. They had free access to water all over the period of the work. The animals were divided into five groups of 10 rats each.

Preparation of the working solutions

Working solution of OB (purchased from AnaSpec, Fermont, California, USA) was made in normal saline (0.9% sodium chloride). One milligram of OB was dissolved in 1 ml saline and a stock solution was prepared and kept at −70°C.

LC was purchased from Arab Company (Cairo, Egypt) for Pharmaceuticals and Medicinal Plants in the form of syrup (300 mg/ml LC). The LC syrup was diluted in a physiological saline solution.

Experimental design

Before the initiation of our study, 10 male rats were used as the control group (group I). This group was fed ad libitum (free access to food and water) standard commercial chow with tap water for 8 weeks. Another 50 rats were prepared to develop obesity by feeding them a hypercaloric diet consisting of 33% standard chow, 33% Nestlé condensed milk (Nestlé, Vevey, Vaud, Switzerland), 7% saccharine, and 27% water for 15 weeks [21]. After this period and according to their weight, 40 obese rats were chosen. Rats were considered obese when their weight exceeds 30% of the original weight [22]. The obese animals are kept on the same diet and were divided into further four groups as follows.

Group II

This group consisted of 10 obese rats that were injected intraperitoneally with saline solution (0.9% NaCl) and were also treated orally with saline by intragastric tube for 8 weeks.

Group III (OB-treated obese rats)

This group consisted of 10 obese rats that were given OB intraperitoneally at a dose of 16 nmol/kg/day as one dose [23] for a period of 8 weeks.

Group IV (LC-treated obese rats)

This group consisted of 10 obese rats that were given LC orally at a dose of 150 mg/kg/day by intragastric tube for a period of 8 weeks [24].

Group V (OB and LC-treated obese rats)

This group consisted of 10 obese rats that were given OB intraperitoneally and LC orally for 8 weeks at the same doses given in group III and IV.

Blood and organs sampling

At the end of the experimental period, the rats were weighed to determine their body weight. Rats were fasted for 12 h, and then fasting blood samples were taken from retro-orbital venous plexus immediately in heparinized capillary tubes under light ether anesthesia. Thereafter, the blood was centrifuged at 3000 rpm for 15 min to separate plasma for different biochemical assays. The animals were then decapitated under ether anesthesia, and tissue samples (from the testis) were rapidly excised and stored at −20°C for subsequent biochemical assays.

Semen sampling and determination of sperm count and motility

The epididymal sperms were collected by cutting epididymis into small pieces and flushing the sperms in normal saline. The sperms were incubated at 32°C, which is the optimum temperature of rat epididymal sperm. The epididymal fluid was diluted to a volume of 5 ml of normal saline (32°C). Epididymal sperm counts and evaluation of their motility were performed according to the method of Seed et al. [25].

Biochemical assays

Plasma TG, total cholesterol (TC), HDL-C, and low-density lipoprotein-cholesterol (LDL-C) levels were determined using Roche Hitachi (Basel, Switzerland) 912 Chemistry Analyzer according to the manufacturer's instructions. Plasma testosterone was measured using mouse and rat testosterone enzyme-linked immunosorbent assay (ELISA) kits supplied by Alpco Immunoassays, USA.

Plasma FSH level was measured by rat FSH ELISA kit. Plasma LH was estimated by rat LH ELISA kit. Both kits were supplied by Elabscience Biotechnology Co. Ltd (Beijing, China).

Thiobarbituric acid reactive substance (TBARS) in testicular tissue was estimated by the method of Ohkawa et al. [26]. Superoxide dismutase (SOD) activity in testicular tissue was measured by the method of Marklund and Marklund [27]. Catalase (CAT) activity in testicular tissue was measured according to the method of Aebi [28]. Activity of glutathione peroxidase (GSH-Px) in testicular tissue was determined according to the method of Lawrence and Burk [29].

Statistical analysis

Data were processed using the statistical package for the social sciences version 20 (SPSS Inc., Chicago, Illinois, USA) program. Descriptive statistics were used as means (M) and SD, frequency distribution, and comparisons. One-way analysis of variance test was used to compare between groups, followed by post-hoc test (least significant difference) for intergroup comparisons. We considered differences to be statistically significant, if P values were less than 0.05.


  Results Top


Effect of obesity and its treatment with obestatin and l-carnitine separately and in combination on body weight and plasma levels of triglycerides, total cholesterol, low-density lipoprotein-cholesterol, and high-density lipoprotein-cholesterol

The results of our study showed that the development of obesity in group II resulted in significant increase in body weight, plasma level of TG, TC, and LDL-C with significant decrease in HDL-C as compared with the control group. Treatment of obese rats with OB alone in group III resulted in significant decrease in body weight, plasma levels of TG, TC, and LDL-C associated with significant elevation in HDL-C. In addition, in group IV the treatment of obese rats with LC alone produced similar significant changes when compared with group II (the obese group). With respect to the effect on body weight, OB produced more reduction in body weight than that produced by LC. Finally, the combined treatment of obese rats with both OB and LC in group V resulted in more significant reduction in plasma levels of TG, TC, and LDL-C and more significant elevation in HDL-C compared with group II [Table 1].
Table 1: Effect of obesity and its treatment with obestatin and L-carnitine separately and in combination on body weight, plasma levels of triglyceride, total cholesterol, high-density lipoprotein-cholesterol, and low-density lipoprotein-cholesterol

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Effect of obesity and its treatment with obestatin and l-carnitine separately and in combination on plasma testosterone, follicle stimulating hormone, and luteinizing hormone levels

When comparing the results in group II (the obese group) with that of group I (the control group), it will be obvious that obesity resulted in significant decrease in plasma testosterone, FSH, and LH levels. In group III, treatment of obese rats with OB produced significant increase in plasma testosterone with insignificant elevation of FSH and LH levels as compared with group II. However, in group IV the administration of LC to the obese rats caused significant elevation in plasma testosterone, FSH, and LH levels as compared with group II. Moreover, treatment of obese rats with combined OB and LC resulted in more significant increase in plasma testosterone and gonadotrophins (FSH and LH) levels when compared with obese untreated rats [Table 2].
Table 2: Effect of obesity and its treatment with obestatin and L-carnitine separately and in combination on plasma testosterone, follicle stimulating hormone, and luteinizing hormone levels

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Effect of obesity and its treatment with obestatin and l-carnitine separately and in combination on tissue levels of thiobarbituric acid reactive substance and enzyme activities of superoxide dismutase, catalase, and glutathione peroxidase in the testis

In group II (the obese group), there was significant increase of TBARS level in testicular tissue indicating increased oxidative stress. In contrast, there was significant reduction of SOD, CAT, and GSH-Px antioxidant enzyme activities in testicular tissue in the same group as compared with the control group. Treatment of obese rats with OB alone in group III produced significant reduction of TBARS level associated with significant elevation of SOD, CAT, and GSH-Px antioxidant enzyme activities in testicular tissue as compared with group II. In addition, LC when given to the obese rats in group IV resulted in significant decrease in TBARS level together with significant increase of SOD, CAT, and GSH-Px antioxidant enzyme activities in testicular tissue when compared with the obese untreated group. The combined treatment with both OB and LC in group V produced more significant changes than those produced in group III and IV, with restoration of the antioxidant enzymes activities to near-normal values [Table 3].
Table 3: Effect of obesity and its treatment with obestatin and l-carnitine separately and in combination on tissue levels of thiobarbituric acid reactive substance and enzyme activities of superoxide dismutase, catalase, and glutathione peroxidase in the testis

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Effect of obesity and its treatment with obestatin and l-carnitine separately and in combination on sperm count and motility

The effect of obesity on sperm count and motility is apparent in [Table 4], which shows that obesity in group II resulted in significant reduction in both sperm count and motility when compared with the control group. In contrast, the administration of OB in group III caused significant elevation in both parameters. Similarly, the treatment of obese rats with LC in group IV produced significant increase in sperm count and motility. Finally, the combined treatment with both OB and LC more significantly increased the sperm count and motility than that produced in group III and group IV. All these results are compared with those of group II [Table 4].
Table 4: Effect of obesity and its treatment with obestatin and L-carnitine separately and in combination on sperm count and motility

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  Discussion Top


Obesity in reproductive-age men has nearly tripled in the past 30 years and coincides with an increase in male infertility worldwide. There is now emerging evidence that male obesity impacts negatively on male reproductive potential not only reducing sperm quality, but also in particular altering the physical and molecular structure of germ cells in the testes, and ultimately mature sperm [4].

The aim of the present study was to investigate the defensive role of OB and LC against reproductive disorders induced by obesity in male rats.

The results of the current study revealed that the animals in group II, the obese nontreated group, had significant increase in body weight. It also showed elevated plasma TG, TC, and LDL-C with decreased HDL-C levels in comparison with the control rats. Exploring the study results showed that the administration of OB or LC alone produced significant decrease in body weight, plasma TG, TC, and LDL-C with increased HDL-C levels with respect to the nontreated group II.

It is interesting to know that the effect of LC was better than that produced by OB on all parameters except the effect of OB on body weight. Finally, combined treatment by both LC and OB produced more significant results.

It was reported that, in obese rats, manifesting insulin resistance, LC supplementation improved glucose tolerance, increased total energy expenditure, reduced fat mass, and increased muscle mass [30]. Furthermore, it was revealed that oral administration of LC caused significant decrease in food intake, whole body weight, and adipose tissue accumulation [31],[32]. All these previously mentioned mechanisms may contribute to weight loss.

In contrast, treatment of obese rats with OB decreased body weight as it suppressed food intake, kept food in the rat's stomach longer, slowed the movement of digested food from the stomach into the intestines, inhibited jejunal contraction, and slowed down again the process of the food passage through the intestines, which led to longer satiety and decreased body weight gain [11],[12].

With respect to the effect of LC on lipid profile, our results are in accordance with Kim and Kim [32] who reported that daily treatment with LC orally for 2 months reduced serum levels of free fatty acids, TG, TC, and VLDL-C and increased HDL-C.

The previous effect can be explained by that LC is essential for b-oxidation of long-chain fatty acids in mitochondria for energy production, with a subsequent reduction in substrate availability for the synthesis of TG in the liver [19].

As it was reported that abnormal lipid and energy metabolism induced by a high-fat diet resulted in fat accumulation by decreased fatty acids oxidation [33], LC administration will be very effective in improving the abnormal lipid metabolism causing obesity.

In addition, the effect of OB on TG, TC, HDL-C, and LDL-C plasma levels observed in the current study was in accordance with other study, which showed that OB treatment of obese rats significantly protects against changes of plasma lipid levels [34].

It was reported that hyperlipidemia and insulin resistance are associated with low serum testosterone level [35],[36]. Accordingly, the reduction in body weight and improvement of lipid profile and insulin resistance caused by the administration of both LC and OB will increase serum testosterone level in obese rats and attenuate the destructive effects of high LDL and oxidized LDL levels on spermatogenesis.

The results of the current study revealed that, in group II, the obese nontreated group, plasma testosterone, FSH, and LH levels were reduced in obese rats. These results are in accordance with many studies that reported the same hormonal changes in cases of obesity [6],[37],[38].

In the present work, it is remarkable that the administration of LC in group IV produced significant increase in plasma testosterone, FSH, and LH levels, whereas OB in group III caused significant elevation in plasma testosterone with nonsignificant increase in plasma FSH and LH levels. Finally, the combined use of both LC and OB in group V produced significant elevation in plasma level of the three hormones. These changes in group V were associated with significant increase in sperm count and motility in the rats' semen and were better results than produced by LC alone.

In rats, LC supplementation increased growth and secretory activity of gonadotropin-releasing hormone (GnRH) cells in vitro and stimulated hypothalamic-pituitary function. It is probable that its effect on gonadotropin release is related to enhancement of GnRH neuronal function in the hypothalamus [39].

In addition, the administration of LC or one of its derivatives, acetyl-LC, has been shown to cause an increase in testosterone levels by increasing nitric oxide (NO) and cyclic guanosine monophosphate levels [40]. NO activates the release of luteinizing hormone-releasing hormone, which activates LH production by the activation of neural NO synthase [41]. In addition, cyclic guanosine monophosphate serves as an intermediate in the signaling cascade that begins with LH binding and results in testosterone production [40].

In the LC-treated group, the data were in accordance with other studies [20],[42],[43] that showed an increase in sperm count, motility, and viability after the administration of LC. Moreover, Garolla et al. [44] reported that the total LC level in seminal plasma of patients with idiopathic oligoasthenospermia was found to be low and oral LC supplementation improved sperm count and motility.

In obesity, there is a possible increase in the secretion of leptin, which has been associated with reduced androgen levels by direct regulation of testicular steroidogenesis by the negative effect of leptin on Leydig cells function [45].

Epididymal sperms use fatty acid oxidation as the main source of energy metabolism. LC is crucial to transport fatty acids into mitochondrial matrix within spermatozoa for energy production needed for sperm maturation and motility. In addition, it has an antioxidant capacity capable of protecting sperms from oxidative damage [42],[43],[46].

Our results reported that plasma testosterone concentrations were found significantly high in the OB-treated obese animals when compared with the obese group (group II). The increase in plasma testosterone level caused by the administration of OB can be explained by its ability to decrease body weight and adipose tissue mass [11]. This increase in the plasma testosterone level will, in turn, cause more reduction in body weight [47] and add to the effect of OB, producing more increase in plasma testosterone level and so on.

Similar results were obtained by Jahan et al. [48] who mentioned that plasma testosterone concentrations were found significantly higher in the OB-treated groups of rats when compared with the control one.

The current study results showed that, in group III, OB administration caused nonsignificant increase of LH and FSH levels and significant increase in testosterone level in plasma. The exact mechanism responsible for such a positive effect of OB on plasma testosterone concentrations remains to be clarified. However, Dong et al. [49] found that the receptors of OB, which are present in the hypothalamus, help the release of GnRH, which controls LH and FSH secretion and in turn controls plasma testosterone level.

The previous effect of OB on plasma testosterone level could be also a direct result of the binding of OB to its receptor in the Leydig cells of the testes, or it could have enhanced the responsiveness of the Leydig cells toward pituitary LH [15].

It was proved that the level of OB in semen was higher versus serum, and linear correlations existed between OB level in serum and in semen. In addition, semen OB levels were positively correlated with sperm concentration and motility [50]. Hence, the decreased serum OB level observed in obesity will be one of the important factors responsible for the decreased sperm count and motility accompanying obesity. Accordingly, the administration of OB to obese person will improve these sperm abnormalities [14],[15].

In a previous study, testicular histomorphometry revealed that OB treatment caused a significant increase in the primary and secondary spermatocytes, spermatids, and Leydig cells population. These findings indicated that OB can be considered as a stimulator of testicular functions [15].

We cannot exclude, however, that the protective effect of OB may result from additional mechanisms not investigated in the present study, such as NO pathway activation [51]. Other results, indeed, indicate that increased NO availability activates the release of LH [41] and attenuates some alterations in metabolism and gene expression associated with insulin resistance induced by a high-fat diet [52].

It is now known that androgen receptors are existed in the adipose tissues. Hence, the sex steroid hormone receptor complex causes activation of the cAMP cascade, which activates hormone-sensitive lipase leading to lipolysis in adipose tissues [53].

Furthermore, testosterone expresses an increased lipolytic potential and depresses lipoprotein lipase activity in adipose cells. In addition, moderate doses of testosterone increase the lipolytic responsiveness to norepinephrine and this will help the reduction in body weight [54].

In group V, the improvement in sperm count and motility could be due to the increase in plasma testosterone, FSH, and LH levels. This improvement designates the synergistic effect of both LC and OB in protecting against the reproductive abnormalities caused by obesity.

Obesity is associated with oxidative stress with the production of reactive oxygen species. An increased oxidative stress causes a greater number of spermatozoa with DNA fragmentation, a greater frequency of single-strand and double-strand DNA breaks, and increased DNA-protein cross-linking [55].

The results of the current study showed that the combined treatment using OB and LC caused a synergistic improvement in the oxidative stress induced by obesity. They decreased the oxidative stress marker TBARS and increased the activity of antioxidant enzymes SOD, CAT, and GSH-Px significantly in the testicular tissue.

Other studies reported that LC improves sperm parameters mainly by increasing the activity of antioxidant enzymes, which is reflected in the increased levels of CAT and SOD and reduced TBARS in the testicular tissue [17],[56].

These increased activities of antioxidant enzymes lead to reduced levels of free radicals available for lipid peroxidation. Consequently, this will reduce the oxidative stress caused by obesity on testicular tissue, which is the main cause of reproductive abnormalities faced in obese male individuals. Finally, this resulted in increased serum testosterone level with improvement of the sperm count and motility as observed in the current study.

Exploring the results illustrates the restorative effect of OB on TBARS and antioxidant enzymes SOD, CAT, and GSH-Px activities. This is in accordance with a previous study that provides the first evidence that peripheral administration of OB exerted potent anti-inflammatory and maintained a balance in oxidant-antioxidant status through the augmentation of endogenous antioxidants and the inhibition of proinflammatory mediators [57].

OB significantly ameliorated clinical and histopathological severity of inflammatory conditions, and this was associated with reduction of lipid peroxidation and enhancement of glutathione synthesis, which has a critical role in oxidative stress as it is the most abundant endogenous intracellular antioxidant [34],[58].

In group V, the combined treatment with OB and LC caused synergistic improvement in the oxidative stress induced by obesity. It decreased the oxidative stress marker TBARS and increased the activity of antioxidant enzymes SOD, CAT, and GSH-Px significantly in the testicular tissue. The increased activities of testicular antioxidant enzymes in group V may have been caused by a synergistic effect of OB and LC on these enzymes.

Finally, the combined treatment by both LC and OB has a defensive role, not merely protective, on male fertility because of their power to face obesity, antioxidant activity, and ability to enhance the secretion of testosterone, which in turn fights against obesity. This is to say that these two substances act as a double-edged sword resisting the negative effects of obesity on male fertility.


  Conclusion Top


The results of the study verified the possible use of OB and LC as a defensive strategy against fertility disorders induced by obesity. In addition, we can conclude that the combined use of both supplements is more effective than their separate use. Moreover, this study showed that both OB and LC have beneficial effects in combating the oxidative stress in obesity. The use of both agents acts as a synergistic combination because OB has the upper hand in combating obesity symptomatically as anorexigenic agent, whereas LC is superior to OB against the cause of fertility disorders when we deal with obesity as a cause of secondary hypogonadism.

Conflicts of interest

There are no conflicts of interest.

 
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