Research Article
Volume 3 Issue 1 - 2017
Effect of Honey on Body Weight, Body Mass Index and Adiposity in High-Fat Diet Fed Wistar Rats
Omotayo O Erejuwa1*, Basil C Ezeokpo2, Ndubuisi N Nwobodo1, Ebere C Asika1, Kenneth I Nwadike3, Nkemjika I Uwaezuoke3, Daniel C Nwachukwu4, Ude N Ude5, Mohd S Abdul Wahab6 and Siti A Sulaiman6
1Department of Pharmacology and Therapeutics, Faculty of Medicine, Ebonyi State University, Abakaliki, Ebonyi State, Nigeria
2Department of Internal Medicine, Faculty of Medicine, Ebonyi State University, Abakaliki, Ebonyi State, Nigeria
3Department of Pharmacology and Therapeutics, College of Medicine, University of Nigeria, Enugu, Enugu State, Nigeria
4Department of Physiology, College of Medicine, University of Nigeria; Enugu, Enugu State, Nigeria
5Department of Obstetrics and Gynaecology, Federal Teaching Hospital, Abakaliki, Ebonyi State, Nigeria
6Department of Pharmacology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia
*Corresponding Author: Omotayo O Erejuwa, Department of Pharmacology and Therapeutics, Faculty of Medicine, Ebonyi State University, Abakaliki, Ebonyi State, Nigeria.
Received: December 30, 2016; Published: January 05, 2017
Citation: Omotayo O Erejuwa., et al. “Effect of Honey on Body Weight, Body Mass Index and Adiposity in High-Fat Diet Fed Wistar Rats”. EC Pharmacology and Toxicology 3.1 (2017): 03-12.
Abstract
Increased consumption of sugars and sweetened beverages contributes to increased prevalence of obesity. The aims of this study were to investigate the effects of honey supplementation on body weight (BW), weight gain, body mass index (BMI) and adiposity in Wistar rats fed a high-fat diet (HFD). The study also investigated if administration of high doses of honey to HFD fed Wistar rats would deteriorate body weight, weight gain, BMI and adiposity. Rats were fed chow or HFD (coconut and olive oil) and 30% sucrose solution for 8 weeks. The animals were then randomly divided into 5 groups. Group 1 (fed chow) was treated with 1.0 ml/kg BW of drinking water. Group 2 (fed HFD and 30% sucrose solution) was treated with 1.0 ml/kg BW of drinking water. Groups 3, 4 and 5 (fed HFD and 30% sucrose solution) were administered 1.0, 2.0 and 3.0 g/kg BW of honey, respectively. The animals were treated for a duration of 6 weeks. Groups 1 and 2-5 were maintained on chow and HFD, respectively during treatment. The HFD fed control rats showed a higher BW (p > 0.05), weight gain (p < 0.01), BMI (p > 0.05), % change in BMI (p > 0.05), BW/body length (BL) (p < 0.05), adiposity index (AI) (p < 0.05) and % change in AI (p < 0.01) compared with chow fed rats. Honey-treated HFD fed rats showed no significant difference in BMI, BW/BL and AI compared with chow fed rats. Honey (1.0 g/kg BW)-treated HFD fed rats had significantly lower BMI (p < 0.01), % change in BMI (p < 0.01), BW/BL (p < 0.05), AI (p < 0.05) and % change in AI (p < 0.01) compared with HFD fed control rats. These results suggested that 1.0 g/kg BW of honey produced beneficial effects on obesity anthropometric parameters including BMI in HFD fed rats.
Keywords: Honey; Body Mass Index; Obesity; Coconut Oil; Olive Oil; Rats
Abbreviations
HFD: High Fat Diet; BW: Body Weight; BMI: Body Mass Index; BL: Body Length; AI: Adiposity Index; CAM: Complementary and Alternative Medicine; SEM: Standard Error of Mean; ANOVA: Analysis of Variance
Introduction
Obesity constitutes a main global health problem and its prevalence has increased considerably in children and adults in both developed and developing countries [1]. Several factors such as increased consumption of sugars, sweetened beverages, highly saturated fats and physical inactivity contribute to increased incidence of overweight and obesity [2-3]. Obesity is characterized by excessive weight gain and adiposity resulting from an imbalance between energy consumption and expenditure. In addition to regular exercise, changes in and dietary habits are vital in the management of obesity [4]. Even though anti-obesity drugs are effective in reducing weight gain, these drugs have low benefit to risk ratio [5]. There is therefore an urgent need for the discovery of additional agents which are more therapeutic and beneficial for obesity. There has been an increased interest in the use of complementary and/or alternative medicine (CAM) for the treatment of various ailments including obesity in the past decade [6-7]. This may be attributed to commonly held beliefs that CAM treatments are safer and cheaper. The accuracy of some of these beliefs still remain controversial especially in view of limited data on the efficacy and safety of CAM [7].
Honey has been used in traditional medicine as far back as 2100 - 2000 BC. The increased patronage of honey in treating diverse ailments in the recent past is attributed to a rise in availability of evidence-based data on the health benefits of honey [8]. Honey has been shown to prevent weight loss or improve weight gain in diabetic rats induced by chemicals such as streptozotocin [9]. Some, other studies found no such effects [10]. The reasons for the inconsistency on the effect of honey on body weight in alloxan- or streptozotocininduced diabetic rats remain unclear. The role of botanical sources and geographical origins of those honeys may be a factor. Alloxan- or streptozotocin-induced diabetes, a model of type 1 diabetes, is associated with weight loss – a consequence of reduced insulin secretion from pancreas [11]. Therefore, prevention of weight loss or promotion of weight gain is a desirable effect of honey in this type of diabetes. There is no doubt that amelioration of hyperglycemia may contribute to body weight improvement in honey-treated diabetic rats. However, reduced hyperglycemia alone does not entirely explain improved weight gain in honey-treated diabetic rats. This is based on the fact that glibenclamide-treated diabetic rats with improved glycemia showed no body weight gain whereas diabetic rats administered glibenclamide and honey exhibited both lower hyperglycemia and improved body weight [12]. This therefore suggests that honey enhances weight gain through a mechanism independent of its hypoglycemic effect.
In healthy rats, the data on the effect of honey on body weight are likewise inconsistent. While most studies showed that honey caused no significant change in body weight in normal rats [13-14] and hypertensive rats [15], honey has been found to promote weight gain in normal rats [10]. In that same study, honey also enhanced weight gain in fructose-fed rats [10]. Compared to sucrose, available data indicated that honey supplementation caused lower weight gain [16-17]. In obesity (a disorder characterized by increased weight gain), the body weight-enhancing effect of honey is undesirable or unwanted. Moreover, if honey ingestion is combined with consumption of HFD or excessive sugar, this potential weight gain-promoting effect of honey may be of grave concern in obesity. As a result of lack of data on the effects of honey on obesity anthropometric parameters, this preliminary study was carried out to investigate the effects of honey supplementation on body weight, weight gain, BMI and adiposity in Wistar rats fed a HFD (an animal model of obesity). The study also investigated if administration of high doses of honey to HFD fed Wistar rats would deteriorate body weight, weight gain, BMI and adiposity.
Materials and Methods
Animals
Male Wistar rats (aged 12 weeks) were purchased from animal house unit, Nsukka, Enugu State, Nigeria. The rats were allowed to acclimatize to the animal room for at least a week. The animal room was well ventilated with temperature of 25-27°C and 12:12-h light:dark cycle. During the one-week acclimatization period, the rats were given free access to rat chow and drinking water ad libitum. The study protocol was approved by University Research Ethics Committee of Ebonyi State University. The animals were humanely handled and in strict compliance with institutional and international guidelines on the Use and Handling of Experimental Animals. The rats (referred to as experimental animals or rats) were fed a HFD and 30% sucrose solution for 8 weeks. The HFD comprised coconut oil and olive oil which were mixed together in the ratio 1:1. The oil was administered to the experimental rats at a dose of 5 ml/kg BW via an oral gavage once daily.
Honey
The honey used in this study was purchased from a bee farm in Abakaliki, Ebonyi State, Nigeria. It was registered with National Agency for Food and Drug Administration Control (NAFDAC). The honey was dissolved in drinking water not more than 30 minutes before administration.
Treatment
At the end of the 8 weeks of feeding with a HFD and 30% sucrose solution, the experimental rats were randomly divided into 4 groups. Each group consisted of five rats. The randomization was performed such that the average body weight of rats in each group was comparable. Another group of rats fed rat chow served as control. The control rats had similar body weight as the experimental groups. Hence, there was no difference in body weight between the experimental and control groups of rats before the commencement of treatment. With the aid of an oral canula, the rats were treated with drinking water or honey once daily for 6 weeks as follows:
Group 1: Chow fed rats administered 1 mL/kg BW of drinking water
Group 2: Experimental rats administered 1 mL/kg BW of drinking water
Group 3: Experimental rats treated with 1.0 g/kg BW of honey
Group 4: Experimental rats treated with 2.0 g/kg BW of honey
Group 5: Experimental rats treated with 3.0 g/kg BW of honey
An hour after treatment each day, the experimental rats were administered the HFD (coconut and olive oil; 5 mL/kg BW). Before the commencement of treatment, body weight and body length of rats were measured using a weighing scale and tape rule, respectively. The measurements obtained were used as baseline data. Thereafter, the body weight was weighed weekly. After treatment for 6 weeks, body weight and body length were measured. The body weight and body length measurements were used for the estimation of BMI and adiposity index. The BMI was determined using the formula: BMI = Body weight (g) / body length2 (cm2). Adiposity index was calculated using the formula for Lee index of obesity: Adiposity index = cube root of body weight (g) / body length (cm) [18]. The rats were sacrificed under diethyl ether anesthesia.
Statistical Analysis
The results were analyzed using SPSS version 16. Data are expressed as mean ± SEM. One-way analysis of variance (ANOVA) and Tukey’s post hoc test were used to assess differences among the groups.
Results and Discussion
Effect of Honey on Body Weight and Weight Gain during the 6 Weeks of Treatment
There was no significant difference in body weight at week 0, 1, 2, 3, 4, 5 and 6 between the HFD fed groups of rats and chow fed rats despite the fact that the HFD fed rats had higher body weight (Figure 1). The body weight was not statistically significantly (p > 0.05) different in the honey-treated HFD fed rats compared with HFD fed control rats though the honey-treated rats had lower body weight than the HFD fed control rats. Total weight gain was significantly (p < 0.01) higher in HFD fed control rats than in chow fed rats (Figure 2). The HFD fed rats treated with 3 g/kg BW of honey showed significantly greater weight gain compared with chow fed rats. Weight gain in HFD fed rats treated with 1 or 2 g/kg BW of honey was not significantly (p > 0.05) different from that of the chow fed rats.

Figure 1: Effect of honey on body weight during the 6 weeks of treatment.

Figure 2: Effect of honey on total weight gain after 6 weeks of treatment.
* p < 0.05 & ** p < 0.01 compared with chow fed rats

Effect of Honey on Body Mass Index and % Change in Body Mass Index after 6 Weeks of Treatment
The BMI was similar among all the groups before treatment (Figure 3). After treatment, BMI was non-significantly (p = 0.069) higher in HFD fed control rats than in chow fed rats. The HFD fed rats treated with 1 g/kg BW of honey had significantly (p < 0.01) lower BMI than HFD fed control rats. The HFD fed rats treated with 2 g/kg BW of honey had borderline (p = 0.058) lower BMI than HFD fed control rats. The HFD fed rats treated with 1 g/kg BW of honey had significantly (p < 0.01) lower % change in BMI compared with HFD fed control rats (Figure 4).

Figure 3: Effect of honey on body mass index after 6 weeks of treatment.
†† p < 0.01 compared with high-fat fed control rats at week 6

Figure 4: Effect of honey on % change in body mass index after 6 weeks of treatment.
†† p < 0.01 compared with high-fat fed control rats

Effect of Honey on Body Weight/Body Length, Adiposity Index and % Change in Adiposity Index after 6 Weeks of Treatment
There was no significant difference in body weight/body length among all the groups before treatment commenced (Figure 5). After treatment, body weight/body length was significantly (p < 0.05) higher in HFD fed control rats than in chow fed rats. The HFD fed rats treated with honey (1 g/kg BW) had significantly (p < 0.05) lower body weight/body length compared with HFD fed control rats. The adiposity index was significantly (p < 0.05) higher in the HFD fed control group than in chow fed rats. The HFD fed rats administered honey (1 g/kg BW) had markedly (p < 0.05) lower adiposity index compared with HFD fed control rats (Figure 6). The % change in adiposity index was significantly (p < 0.01) greater in HFD fed control rats than in chow fed rats (Figure 7). Honey (1 g/kg BW) supplementation produced significantly (p < 0.01) lower % change in adiposity index.

Figure 5: Effect of honey on body weight/body length after 6 weeks of treatment.
* p < 0.05 compared with chow fed rats at week 6; † p < 0.05 compared with high-fat fed control rats at week 6

Figure 6: Effect of honey on adiposity index after 6 weeks of treatment.
* p < 0.05 compared with chow fed rats at week 6; † p < 0.05 compared with high-fat fed control rats at week 6

Figure 7: Effect of honey on % change in adiposity index after 6 weeks of treatment.
** p < 0.01 compared with chow fed rats; †† p < 0.01 compared with high-fat fed control rats

This study investigated the effects of honey on body weight, weight gain, BMI and adiposity in HFD fed Wistar rats. The potential deteriorating effects of high doses of honey on body weight, weight gain, BMI and adiposity in HFD fed Wistar rats were also assessed. To the best of the authors’ knowledge, it is worth mentioning that this is the first study to investigate the effects of honey in HFD fed rats (a rodent model of obesity). The results showed that the Wistar rats fed HFD had non-significant greater body weight than chow fed rats starting from week 1 till week 6. Total weight gain over the period of 6 weeks was significantly higher in HFD fed control rats than in chow fed rats. These observations are similar to previous reports that demonstrated higher body weight and/or total weight gain in rats fed HFD [19-20]. Beginning from week 2, all the honey-supplemented HFD fed groups of rats exhibited non-significantly lower body weight compared with the HFD fed control rats. With the exception of the HFD fed rats treated with 3 g/kg BW of honey, the total weight gain in the honey-treated HFD fed rats was not significantly different from that of the chow fed rats. These data corroborate previous findings showing that honey administration to healthy rats resulted in lower body weight and weight gain [16,21]. The findings on body weight and total weight gain revealed that the lower the dose, the greater the suppressing effect of honey. With respect to this negative dose dependent effect of honey on body weight and total weight gain in HFD fed rats, it is difficult to draw a comparison with previous studies. This is because no study has determined the effect of honey in HFD fed rats. Similarly, previous studies that investigated the effect of honey in fructose-fed rats or compared the effect of honey with other sugars on body weight and weight gain in healthy rats utilized only one dose of honey [10,16-17].
The study found non-significantly higher BMI in HFD fed control rats than in chow fed rats. Other previous reports have also documented non-significantly or significantly higher BMI in HFD fed rats [22-23]. In humans, BMI reflects fat mass and a higher BMI is associated with an increased cardiovascular risk and all-cause mortality [24]. All the honey-supplemented HFD fed rats had comparable BMI as the chow fed rats. Similar to data on weight gain, the results of the effect of honey on BMI in HFD fed rats indicated a lower dose-greater response relationship. This negative dose dependent effect of honey on BMI in HFD fed rats is reinforced by the fact that the HFD fed rats treated with 1 g/kg BW of honey showed significantly lower BMI compared with the HFD fed control rats. The % change in BMI in HFD fed control rats was non-significantly higher than in chow fed rats. The HFD fed rats treated with honey showed similar % change in BMI as the chow fed rats. The lowest dose of honey produced a significant lower % change in BMI compared with the HFD fed control group, a demonstration of negative dose dependent effect of honey on % change in BMI.
Like the BMI, the body weight/body length and adiposity index represent additional indicators of body fatness. Higher adiposity has been demonstrated in HFD fed rats [23]. In this study, the body weight/body length and adiposity index were significantly higher in HFD fed control group than in chow fed group. The % change in adiposity index was also significantly higher in the HFD fed control group than in chow fed group. These data are in agreement with previous findings [23,25]. Administration of honey suppressed body weight/body length, adiposity index and % change in adiposity index towards those of the chow fed rats. However, of the three administered doses of honey, only 1 g/kg BW dose produced significantly lower body weight/body length, adiposity index and % change in adiposity index compared with the HFD fed control rats. These data are again consistent with the results on weight gain and BMI demonstrating a negative dose response relationship. At the moment, it remains unclear if the negative dose response of honey on weight gain, BMI and adiposity in Wistar rats fed HFD would also manifest on the lipid profile. Additional research is needed to clarify this even though there is a positive correlation between BMI and triglycerides [26].
The issue of negative dose-dependent effects of honey on all the parameters examined in this study becomes relevant in view of previously reported findings and propositions. In a previous study, honey supplementation was found to exert a dose-dependent hypoglycemic or glucose-lowering effect [27]. However, the maximal dose for the glucose-lowering effect of honey was recently reported [28]. Honey is predominantly sugars – consisting primarily of fructose and glucose as well as other classes of carbohydrate including disaccharides and oligosaccharides. Some of these sugars especially fructose and oligosaccharides are proposed to contribute to glucose-lowering effect of honey [29-30]. It is therefore not surprising that increasing the dose of honey resulted in greater lowering of hyperglycemia in diabetic rats [27]. That is, honey administration demonstrated a positive (glucose-lowering) dose response relationship in diabetic rats. This is in contrast to negative dose response found in HFD fed rats in this study. It is worthy of note that in spite of this negative dose-dependent effect of honey in obese rats, neither 2 nor 3 g/kg BW of honey caused greater body weight, weight gain, BMI or adiposity in HFD fed rats compared with HFD fed control rats. Based on existing data in the literature, honey is considered a better alternative to artificial sweeteners in diabetic diets [31-32]. The fact that high doses of honey (2 or 3 g/kg BW) did not deteriorate obesity parameters as observed in this study suggests that honey has a potential to serve as a viable functional food or substitute to synthetic sweeteners in obese diets.
The role of fructose in the development of obesity still remains controversial. Findings from animal studies revealed that administration of high doses of fructose is detrimental to health and may enhance the development of obesity features [33-34]. In humans, while evidence suggests that fructose (if consumed within the normal and accepted range of human consumption) may not constitute an increased risk of obesity [2], several studies have demonstrated the beneficial effects of fructose restriction or reduction in obese subjects [35-36]. By and large, in spite of the debate on the association of fructose with obesity, there seems to be convincing evidence in support of the benefits of lower doses of fructose or fructose reduction in obesity. This is important with regards to the data obtained in this study. As reported, neither 2 nor 3 g/kg BW of honey produced a significantly lower BMI, % change in BMI, body weight / body length, adiposity index and % change in adiposity index compared with HFD fed control rats. In contrast, significantly beneficial effects of 1 g/kg BW of honey on these obesity parameters were demonstrated. Therefore, it is possible that at high doses, the high sugar content of honey especially fructose may render honey less beneficial in obesity. This may provide a plausible explanation for the negative dose response of honey observed in this study.
It is important to note that obesity is a lifestyle and chronic disorder. Hence, its treatment requires a long-term intervention. In such a chronic disorder, despite the positive beneficial effects of honey demonstrated in this study, 6 weeks of honey supplementation may be considered inadequate or acute. This view is based on the findings from a previous study which showed that the acute beneficial effects of honey might not be observed in a chronic study [37]. The researchers reported that rats administered honey (500 or 800 mg) for 2 days had significantly higher calcium absorption. In contrast, long-term (8 weeks) honey administration showed no such effect. Consequently, studies on long-term effects of honey supplementation in HFD fed rats are recommended. Such studies are necessary to demonstrate the sustainability of the reported beneficial effects of honey on weight gain, BMI and adiposity in HFD fed rats. Besides, considering that variations in honey composition (which influence its biological responses) pose a great challenge to reproducibility [8], it is recommended that further studies that utilize honeys of other botanical or geographical sources are also carried out to confirm the reproducibility of these findings.
Conclusions
This study showed that 6 weeks of honey supplementation resulted in beneficial effects of honey (1 g/kg BW) on obesity parameters in HFD fed Wistar rats. The study revealed that high doses of honey (2 or 3 g/kg BW) did not increase body weight, weight gain, BMI and adiposity. However, the findings indicated that honey supplementation exerted a negative dose response in an animal model of obesity. By and large, it can be suggested that honey has a potential to serve as a viable functional food or a substitute for artificial/synthetic sweeteners in obese diets. Long-term studies are needed to demonstrate the sustainability of these reported beneficial effects of honey in HFD fed rats. Further studies that utilize honeys of other botanical and/or geographical sources are also desirable to confirm the reproducibility of these findings.
Acknowledgements
This study was supported by financial contributions from all the authors.
Conflict of Interest
The authors declare that there is no conflict of interest.
Bibliography
  1. Ng M., et al. “Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013”. Lancet 384.9945 (2014): 766-781.
  2. Rippe JM., et al. “Added sugars and risk factors for obesity, diabetes and heart Disease”. International Journal of Obesity 40.1 (2016): S22-S27.
  3. Myers A., et al. “Associations among sedentary and active behaviours, body fat and appetite dysregulation: investigating the myth of physical inactivity and obesity”. British Journal of Sports Medicine (2016).
  4. Armenta Guirado BI., et al. “[Obesity management in the primary care setting by an intensive lifestyle intervention]. Nutricion Hospitalaria 32.4 (2015): 1526-1534.
  5. Kang JG., et al. “Anti-obesity drugs: a review about their effects and safety”. Diabetes and Metabolism Journal 36.1 (2012): 13-25.
  6. Shively CD. “What’s the difference between complementary and alternative health approaches?”. EC Pharmacology and Toxicology 1.1 (2016): 13-14.
  7. Esteghamati A., et al. “Complementary and alternative medicine for the treatment of obesity: a critical review”. nternational Journal of Endocrinology and Metabolism 13.2 (2015): e19678.
  8. Erejuwa OO. “Effect of honey in diabetes mellitus: matters arising”. Journal of Diabetes and Metabolic Disorder 13 (2014): 23.
  9. Erejuwa OO., et al. “Effects of Malaysian tualang honey supplementation on glycemia, free radical scavenging enzymes and markers of oxidative stress in kidneys of normal and streptozotocin-induced diabetic rats”. International Journal of Cardiology 137.1 (2009): S45.
  10. Fasanmade AA., et al. “Differential effect of honey on selected variables in alloxan-induced and fructose-induced diabetic rats”. African Journal of Biomedical Research 11.2 (2008): 191-196.
  11. Szkudelski T. “The mechanism of alloxan and streptozotocin action in B cells of the rat pancreas”. Physiological Research 50.6 (2001): 537-546.
  12. Erejuwa OO., et al. “Effect of glibenclamide alone versus glibenclamide and honey on oxidative stress in pancreas of streptozotocininduced diabetic rats”. International Journal of Applied Research in Natural Products 4.2 (2011): 1-10.
  13. Aziz CB., et al. “The antinociceptive effects of tualang honey in male sprague-dawley rats: a preliminary study”. Journal of Traditional and Complementary Medicine 4.4 (2014): 298-302.
  14. Erejuwa OO., et al. “Glibenclamide or metformin combined with honey improves glycemic control in streptozotocin-induced diabetic rats”. International Journal of Biological Sciences 7.2 (2011): 244-252.
  15. Erejuwa OO., et al. “Honey supplementation in spontaneously hypertensive rats elicits antihypertensive effect via amelioration of renal oxidative stress”. Oxidative Medicine and Cellular Longevity (2012): 374037.
  16. Chepulis LM. “The effect of honey compared to sucrose, mixed sugars, and a sugar-free diet on weight gain in young rats”. Journal of Food Sciences 72.3 (2007): S224-S229.
  17. Nemoseck TM., et al. “Honey promotes lower weight gain, adiposity, and triglycerides than sucrose in rats”. Nutrition Research 31.1 (2011): 55-60.
  18. Bernardis LL. “Prediction of carcass fat, water and lean body mass from Lee’s “nutritive ratio in rats with hypothalamic obesity”. Experientia 26.7 (1970): 789-790.
  19. Tseng SH., et al. “Hypolipidemic effects of three purgative decoctions”. Evidence-Based Complementary and Alternative Medicine (2011): 249254.
  20. Sandoval-Salazar C., et al. A high-fat diet decreases GABA concentration in the frontal cortex and hippocampus of rats”. Biological Research 49 (2016): 15.
  21. Chepulis L., et al. “The long-term effects of feeding honey compared with sucrose and a sugar-free diet on weight gain, lipid profiles, and DEXA measurements in rats” Journal of Food Science 73.1 (2008): H1-H7.
  22. Altunkaynak ME., et al. “The effects of high-fat diet on the renal structure and morphometric parametric of kidneys in rats”. Journal of Anatomy 212.6 (2008): 845-852.
  23. Sinitskaya N., et al. “Increasing the fat-to-carbohydrate ratio in a high-fat diet prevents the development of obesity but not a prediabetic state in rats”. Clinical Science (London) 113.10 (2007): 417-425.
  24. Twig G., et al. “Body-Mass Index in 2.3 Million Adolescents and Cardiovascular Death in Adulthood”. The New England Journal of Medicine 374.25 (2016): 2430-2440.
  25. Fernandez CD., et al. “Diet-induced obesity in rats leads to a decrease in sperm motility”. Reproductive Biology and Endocrinology 9 (2011): 32.
  26. Novelli EL., et al. “Anthropometrical parameters and markers of obesity in rats”. Laboratory Animals 41.1 (2007): 111-119.
  27. Erejuwa OO., et al. “Hypoglycemic and antioxidant effects of honey supplementation in streptozotocin-induced diabetic rats”. International Journal for Vitamin and Nutrition Research 80.1 (2010): 74-82.
  28. Erejuwa OO., et al. “Nigerian honey ameliorates hyperglycemia and dyslipidemia in alloxan-induced diabetic rats”. Nutrients 8.3 (2016): 95.
  29. Erejuwa OO., et al. “Oligosaccharides might contribute to the antidiabetic effect of honey: a review of the literature”. Molecules 17.1 (2011): 248-266.
  30. Erejuwa OO., et al. “Fructose might contribute to the hypoglycemic effect of honey”. Molecules 17.2 (2012): 1900-1915.
  31. Abdulrhman M., et al. “The glycemic and peak incremental indices of honey, sucrose and glucose in patients with type 1 diabetes mellitus: effects on C-peptide level-a pilot study”. Acta Diabetologica 48.2 (2011): 89-94.
  32. Erejuwa OO., et al. “Honey--a novel antidiabetic agent”. International Journal of Biological Sciences8.6 (2012): 913-934.
  33. Bocarsly ME., et al. “High-fructose corn syrup causes characteristics of obesity in rats: increased body weight, body fat and triglyceride levels”. Pharmacology, Biochemistry, and Behavior97.1 (2010): 101-106.
  34. Saad AF., et al. “High-fructose diet in pregnancy leads to fetal programming of hypertension, insulin resistance, and obesity in adult offspring”. American Journal of Obstetrics and Gynecology 215.3 (2016): 378.e1-378.e6.
  35. Lustig RH.,et al. “Isocaloric fructose restriction and metabolic improvement in children with obesity and metabolic syndrome”. Obesity (Silver Spring)24.2 (2016): 453-460.
  36. Gugliucci A., et al. “Short-term isocaloric fructose restriction lowers apoC-III levels and yields less atherogenic lipoprotein profiles in children with obesity and metabolic syndrome”. Atherosclerosis253 (2016): 171-177.
  37. Ariefdjohan MW., et al. Acute and chronic effects of honey and its carbohydrate constituents on calcium absorption in rats”. Journal of Agricultural and Food Chemistry 56.8 (2008): 2649-2654.
Copyright: © 2017 Omotayo O Erejuwa., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

PubMed Indexed Article


EC Pharmacology and Toxicology
LC-UV-MS and MS/MS Characterize Glutathione Reactivity with Different Isomers (2,2' and 2,4' vs. 4,4') of Methylene Diphenyl-Diisocyanate.

PMID: 31143884 [PubMed]

PMCID: PMC6536005


EC Pharmacology and Toxicology
Alzheimer's Pathogenesis, Metal-Mediated Redox Stress, and Potential Nanotheranostics.

PMID: 31565701 [PubMed]

PMCID: PMC6764777


EC Neurology
Differences in Rate of Cognitive Decline and Caregiver Burden between Alzheimer's Disease and Vascular Dementia: a Retrospective Study.

PMID: 27747317 [PubMed]

PMCID: PMC5065347


EC Pharmacology and Toxicology
Will Blockchain Technology Transform Healthcare and Biomedical Sciences?

PMID: 31460519 [PubMed]

PMCID: PMC6711478


EC Pharmacology and Toxicology
Is it a Prime Time for AI-powered Virtual Drug Screening?

PMID: 30215059 [PubMed]

PMCID: PMC6133253


EC Psychology and Psychiatry
Analysis of Evidence for the Combination of Pro-dopamine Regulator (KB220PAM) and Naltrexone to Prevent Opioid Use Disorder Relapse.

PMID: 30417173 [PubMed]

PMCID: PMC6226033


EC Anaesthesia
Arrest Under Anesthesia - What was the Culprit? A Case Report.

PMID: 30264037 [PubMed]

PMCID: PMC6155992


EC Orthopaedics
Distraction Implantation. A New Technique in Total Joint Arthroplasty and Direct Skeletal Attachment.

PMID: 30198026 [PubMed]

PMCID: PMC6124505


EC Pulmonology and Respiratory Medicine
Prevalence and factors associated with self-reported chronic obstructive pulmonary disease among adults aged 40-79: the National Health and Nutrition Examination Survey (NHANES) 2007-2012.

PMID: 30294723 [PubMed]

PMCID: PMC6169793


EC Dental Science
Important Dental Fiber-Reinforced Composite Molding Compound Breakthroughs

PMID: 29285526 [PubMed]

PMCID: PMC5743211


EC Microbiology
Prevalence of Intestinal Parasites Among HIV Infected and HIV Uninfected Patients Treated at the 1o De Maio Health Centre in Maputo, Mozambique

PMID: 29911204 [PubMed]

PMCID: PMC5999047


EC Microbiology
Macrophages and the Viral Dissemination Super Highway

PMID: 26949751 [PubMed]

PMCID: PMC4774560


EC Microbiology
The Microbiome, Antibiotics, and Health of the Pediatric Population.

PMID: 27390782 [PubMed]

PMCID: PMC4933318


EC Microbiology
Reactive Oxygen Species in HIV Infection

PMID: 28580453 [PubMed]

PMCID: PMC5450819


EC Microbiology
A Review of the CD4 T Cell Contribution to Lung Infection, Inflammation and Repair with a Focus on Wheeze and Asthma in the Pediatric Population

PMID: 26280024 [PubMed]

PMCID: PMC4533840


EC Neurology
Identifying Key Symptoms Differentiating Myalgic Encephalomyelitis and Chronic Fatigue Syndrome from Multiple Sclerosis

PMID: 28066845 [PubMed]

PMCID: PMC5214344


EC Pharmacology and Toxicology
Paradigm Shift is the Normal State of Pharmacology

PMID: 28936490 [PubMed]

PMCID: PMC5604476


EC Neurology
Examining those Meeting IOM Criteria Versus IOM Plus Fibromyalgia

PMID: 28713879 [PubMed]

PMCID: PMC5510658


EC Neurology
Unilateral Frontosphenoid Craniosynostosis: Case Report and a Review of the Literature

PMID: 28133641 [PubMed]

PMCID: PMC5267489


EC Ophthalmology
OCT-Angiography for Non-Invasive Monitoring of Neuronal and Vascular Structure in Mouse Retina: Implication for Characterization of Retinal Neurovascular Coupling

PMID: 29333536 [PubMed]

PMCID: PMC5766278


EC Neurology
Longer Duration of Downslope Treadmill Walking Induces Depression of H-Reflexes Measured during Standing and Walking.

PMID: 31032493 [PubMed]

PMCID: PMC6483108


EC Microbiology
Onchocerciasis in Mozambique: An Unknown Condition for Health Professionals.

PMID: 30957099 [PubMed]

PMCID: PMC6448571


EC Nutrition
Food Insecurity among Households with and without Podoconiosis in East and West Gojjam, Ethiopia.

PMID: 30101228 [PubMed]

PMCID: PMC6086333


EC Ophthalmology
REVIEW. +2 to +3 D. Reading Glasses to Prevent Myopia.

PMID: 31080964 [PubMed]

PMCID: PMC6508883


EC Gynaecology
Biomechanical Mapping of the Female Pelvic Floor: Uterine Prolapse Versus Normal Conditions.

PMID: 31093608 [PubMed]

PMCID: PMC6513001


EC Dental Science
Fiber-Reinforced Composites: A Breakthrough in Practical Clinical Applications with Advanced Wear Resistance for Dental Materials.

PMID: 31552397 [PubMed]

PMCID: PMC6758937


EC Microbiology
Neurocysticercosis in Child Bearing Women: An Overlooked Condition in Mozambique and a Potentially Missed Diagnosis in Women Presenting with Eclampsia.

PMID: 31681909 [PubMed]

PMCID: PMC6824723


EC Microbiology
Molecular Detection of Leptospira spp. in Rodents Trapped in the Mozambique Island City, Nampula Province, Mozambique.

PMID: 31681910 [PubMed]

PMCID: PMC6824726


EC Neurology
Endoplasmic Reticulum-Mitochondrial Cross-Talk in Neurodegenerative and Eye Diseases.

PMID: 31528859 [PubMed]

PMCID: PMC6746603


EC Psychology and Psychiatry
Can Chronic Consumption of Caffeine by Increasing D2/D3 Receptors Offer Benefit to Carriers of the DRD2 A1 Allele in Cocaine Abuse?

PMID: 31276119 [PubMed]

PMCID: PMC6604646


EC Anaesthesia
Real Time Locating Systems and sustainability of Perioperative Efficiency of Anesthesiologists.

PMID: 31406965 [PubMed]

PMCID: PMC6690616


EC Pharmacology and Toxicology
A Pilot STEM Curriculum Designed to Teach High School Students Concepts in Biochemical Engineering and Pharmacology.

PMID: 31517314 [PubMed]

PMCID: PMC6741290


EC Pharmacology and Toxicology
Toxic Mechanisms Underlying Motor Activity Changes Induced by a Mixture of Lead, Arsenic and Manganese.

PMID: 31633124 [PubMed]

PMCID: PMC6800226


EC Neurology
Research Volunteers' Attitudes Toward Chronic Fatigue Syndrome and Myalgic Encephalomyelitis.

PMID: 29662969 [PubMed]

PMCID: PMC5898812


EC Pharmacology and Toxicology
Hyperbaric Oxygen Therapy for Alzheimer's Disease.

PMID: 30215058 [PubMed]

PMCID: PMC6133268


News and Events


September Issue Release

We always feel pleasure to share our updates with you all. Here, notifying you that we have successfully released the September issue of respective journals and can be viewed in the current issue pages.

Submission Deadline for October Issue

Ecronicon delightfully welcomes all the authors around the globe for effective collaboration with an article submission for the November issue of respective journals. Submissions are accepted on/before October 07, 2020.

Certificate of Publication

Ecronicon honors with a "Publication Certificate" to the corresponding author by including the names of co-authors as a token of appreciation for publishing the work with our respective journals.

Best Article of the Issue

Editors of respective journals will always be very much interested in electing one Best Article after each issue release. The authors of the selected article will be honored with a "Best Article of the Issue" certificate.

Certifying for Review

Ecronicon certifies the Editors for their first review done towards the assigned article of the respective journals.

Latest Articles

The latest articles will be updated immediately on the articles in press page of the respective journals.

Immediate Assistance

The prime motto of this team is to clarify all the queries without any delay or hesitation to avoid the inconvenience. For immediate assistance on your queries please don't hesitate to drop an email to editor@ecronicon.uk