Dear Label_Name,

Greetings! I hope you are well.

I am writing on behalf of an international publishing house, Science and Education Publishing, USA (http://www.sciepub.com).

Science and Education Publishing (SciEP) is a multidisciplinary open access publisher of Journals covering the fields of Science, Technology and Medicine. All SciEP publications are subject to high-quality peer review, editorial and production processes and are freely available online.

Welcome to the April, 2013 edition of SciEP newsletter, providing monthly summaries of articles on science & education related topics of interest to scientist and professionals. The mission of our journals is to provide an open access forum for publishing new findings on issues pertinent to scientific and academic field. We also invite you to submit original research papers, review articles, short reports, or case studies are considered for publication in our Multidisciplinary Journals.

American Journal of Public Health Research
DOI: 10.12691/ajphr-1-1-3

The Implementation of a Tele-Homecare System with Service Oriented Architecture and HL7 Message Transmission Standard
Ching-Sung Wang

American Journal of Medical and Biological Research
DOI: 10.12691/ajmbr-1-1-2

The Influence of Ethanol on Pyruvate Kinases Activity in Vivo, in Vitro, in Silico
Lelevich Sergey Vladimirovich, Khrustalev Vladislav Victorovich, Barkovsky Eugene Victorovich, Shedogubova Tatyana Aleksandrovna

American Journal of Medical Sciences and Medicine
DOI: 10.12691/ajmsm-1-1-1

Clinical and Histological Features in Wegener Granulomatosis
Li Cavoli Gioacchino, Passantino Rita, Bono Luisa, Tortorici Calogera, Ferrantelli Angelo, Giammarresi Carlo, Rotolo Ugo

American Journal of Infectious Diseases and Microbiology
DOI: 10.12691/ajidm-1-1-2

The Curse of Lymphatic Filariasis: Would the Continual Use of Diethylcarbamazine Eliminate this Scourge in Papua New Guinea?
Anne Lanham, Lillian Mwanri

We have released issues of some journals on February 2013.
American Journal of Public Health Research
American Journal of Medical Sciences and Medicine
American Journal of Medical and Biological Research
American Journal of Pharmacological Sciences
American Journal of Clinical Medicine Research
American Journal of Nursing Research
American Journal of Cancer Prevention
American Journal of Medicine Studies
American Journal of Infectious Diseases and Microbiology
American Journal of Cardiovascular Disease Research
American Journal of Biomedical Research
American Journal of Mechanical Engineering
American Journal of Microbiological Research
Journal of Preventive Medicine
American Journal of Food and Nutrition
American Journal of Hypertension Research
American Journal of Sports Science and Medicine
Journal of Cancer Research and Treatment
American Journal of Zoological Research
Journal of Biomedical Engineering and Technology
American Journal of Microbiological Research
Biomedical Science and Engineering

We are pleased to announce that submissions are now being accepted for peer review for all the journals across all our subject areas in SciEP.

Please submit your manuscript via our online submission system:
http://www.sciepub.com/author/signin

To unsubscribe from our mailing list, please click on the following link: unsubscribe

I am looking forward to hearing from you.

Kind regards,

David Rain
Email:join@sciepub.com
Science and Education Publishing (http://www.sciepub.com)

Label_Title

Dear Label_Name,

Greetings! I hope you are well.

I am writing on behalf of an international publishing house, Science and Education Publishing, USA (http://www.sciepub.com).

Science and Education Publishing (SciEP) is a multidisciplinary open access publisher of Journals covering the fields of Science, Technology and Medicine. All SciEP publications are subject to high-quality peer review, editorial and production processes and are freely available online.

Welcome to the April, 2013 edition of SciEP newsletter, providing monthly summaries of articles on science & education related topics of interest to scientist and professionals. The mission of our journals is to provide an open access forum for publishing new findings on issues pertinent to scientific and academic field. We also invite you to submit original research papers, review articles, short reports, or case studies are considered for publication in our Multidisciplinary Journals.

American Journal of Public Health Research
DOI: 10.12691/ajphr-1-1-3

The Implementation of a Tele-Homecare System with Service Oriented Architecture and HL7 Message Transmission Standard
Ching-Sung Wang

American Journal of Medical and Biological Research
DOI: 10.12691/ajmbr-1-1-2

The Influence of Ethanol on Pyruvate Kinases Activity in Vivo, in Vitro, in Silico
Lelevich Sergey Vladimirovich, Khrustalev Vladislav Victorovich, Barkovsky Eugene Victorovich, Shedogubova Tatyana Aleksandrovna

American Journal of Medical Sciences and Medicine
DOI: 10.12691/ajmsm-1-1-1

Clinical and Histological Features in Wegener Granulomatosis
Li Cavoli Gioacchino, Passantino Rita, Bono Luisa, Tortorici Calogera, Ferrantelli Angelo, Giammarresi Carlo, Rotolo Ugo

American Journal of Infectious Diseases and Microbiology
DOI: 10.12691/ajidm-1-1-2

The Curse of Lymphatic Filariasis: Would the Continual Use of Diethylcarbamazine Eliminate this Scourge in Papua New Guinea?
Anne Lanham, Lillian Mwanri

We have released issues of some journals on February 2013.
American Journal of Public Health Research
American Journal of Medical Sciences and Medicine
American Journal of Medical and Biological Research
American Journal of Pharmacological Sciences
American Journal of Clinical Medicine Research
American Journal of Nursing Research
American Journal of Cancer Prevention
American Journal of Medicine Studies
American Journal of Infectious Diseases and Microbiology
American Journal of Cardiovascular Disease Research
American Journal of Biomedical Research
American Journal of Mechanical Engineering
American Journal of Microbiological Research
Journal of Preventive Medicine
American Journal of Food and Nutrition
American Journal of Hypertension Research
American Journal of Sports Science and Medicine
Journal of Cancer Research and Treatment
American Journal of Zoological Research
Journal of Biomedical Engineering and Technology
American Journal of Microbiological Research
Biomedical Science and Engineering

We are pleased to announce that submissions are now being accepted for peer review for all the journals across all our subject areas in SciEP.

Please submit your manuscript via our online submission system:
http://www.sciepub.com/author/signin

To unsubscribe from our mailing list, please click on the following link: unsubscribe

I am looking forward to hearing from you.

Kind regards,

David Rain
Email:join@sciepub.com
Science and Education Publishing (http://www.sciepub.com)

Study on Healing Effects of Bifidobacterium Infantis 35624 in Inflammatory and Energy Metabolism Parameters in High-Fat-Diet-Induced Obesity in Rat Model

Özlem Özdemir*, Çağrı Akalın, Fuat Ekiz, Orhan Baş, Tülin Bayrak

Department of InternalMedicine. MedicineFaculty of Ordu University, Ordu, Turkey

Abstract: Obesity is characterized by increased adipose tissue and low grade inflammation. The gut microbiota is closely associated with the obesity pathophysiology, so the probiotics; living microorganisms are questioned in terms of their effects on obesity related changes. Bifidobacterium infantis 35624 is used as a probiotic supplement in cases of digestive disorders. The aim of this study is to investigate its healing effect on the morphometric and inflammatory-energy metabolism responses in a high-fat diet-induced obese rat model. Three different nutritional groups, each consisting of eight rats, were followed for eight weeks. They received a conventional balanced diet, high-fat diet (HFD), and HFD with the supplementation of Bifidobacterium infantis 35624 respectively. The weight measurements were made weekly. At the end of the study, weight gains and body mass indexes were calculated. Plasma glucose, insulin, interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α) and glucagon-like peptide-1 (GLP-1) levels were evaluated. The weight changes of the HFD group showed a significant difference (p<0.001). HFD group with Bifidobacterium infantis 35624 supplementation showed significantly decreased body weight (p<0,001) and decreased plasma glucose, insulin, IL-6, TNF- α, GLP-1 levels compared to HFD group without probiotic supplementation (p<0,05). Bifidobacterium infantis 35624 may be a candidate probiotic to use in obesity management studies to maintain body weight, host energy metabolism, and inflammatory cytokine levels in high-fat diet nutrition.

Keywords: High-fat-diet, Bifidobacterium infantis 35624, Interleukin-6, Tumor necrosis factor alpha, Obesity, Glucagon-like peptide-1

Received August 15, 2025; Revised September 17, 2025; Accepted September 25, 2025

Citation: Özlem Özdemir, Çağrı Akalın, Fuat Ekiz, Orhan Baş, Tülin Bayrak, Study on Healing Effects of Bifidobacterium Infantis 35624 in Inflammatory and Energy Metabolism Parameters in High-Fat-Diet-Induced Obesity in Rat Model. Journal of Food and Nutrition Research, 13 (9). 364-370. January 2025. doi:10.12691/jfnr-13-9-4

1. Introduction

Obesity is an increasing health problem affecting 30% of the world's population. It is associated with glucose intolerance, insulin resistance, fatty liver disease, and cardiovascular disease [1]. When there is an imbalance between energy intake and energy expenditure, obesity develops as a result of cellular lipid accumulation and increased adipose tissue with low-grade inflammation [2]. The main indicator of the energy metabolism glucagon-like peptide-1 (GLP-1) is mainly expressed in the gastrointestinal system. The main cytokines involved in inflammatory and immune responses are interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha). These parameters are mentioned as powerful markers in the pathophysiology of obesity [3,4]. Again, recent studies have shown that the gut microbiota has an impact beyond digestion. It has been found to play a prominent role in immune and inflammatory events, and changes in this microbiota have been associated with obesity and metabolic disorders [5]. Bifidobacteria species are gram-positive, immobile and anaerobic bacteria. They constitute one of the main groups of bacteria in gut microbiota and they are used by the food industry as probiotic microorganisms in recent years, as some strains have been shown to have some beneficial effects [6]. Probiotics are described as living microorganisms that can influence and protect the natural composition of gut microbiota and contribute to human health. Their benefits, such as facilitating digestion, weight change and supporting immunity, have been reported [7]. Bifidobacterium infantis 35624 is in clinical use as a probiotic formula for dyspepsia and irritable bowel syndrome [8]. But, no study has yet been observed about its effect on obesity in the literature, and this study has been planned with the aim of addressing this deficiency. We evaluated the morphometric, biochemical, and inflammatory-energy metabolism responses in high-fat-diet-induced obesity. Additionally, we examined IL-6, TNF-α, and GLP-1 levels with high-fat diet and the probiotic Bifidobacterium Infantis 35624 supplementation.

2. Materials and Methods

2.1. Ethical Considerations

This study was carried out in accordance with the recommendations of the guide “Regulation on Experimental Animals” (Republic of Turkey). The protocol of the study was approved by the Animal Experiments Local Ethics Committee of Ordu University (16/02/2021, no: 82678388)

2.2. Animal Model and Dietary Interventions

Twenty-week-old male Sprague Dawley (SD) rats weighing 250-300 g (n =24) were obtained from the Experimental Animals Application and Research Center of Ondokuz Mayıs University, Samsun, Turkey. All rats were kept in an air-conditioned room with a 12-hour light and dark cycle at constant temperature and humidity (23 ±1 °C and 55-65%, respectively). Free access to food and water has been provided. After one week of adaptation, rats were randomly divided into three groups (n =8) which fed a normal-fat diet (NFD), a high-fat diet (HFD), and a HFD with probiotic supplementation (HPFD). NFD was a standard feed diet containing 10% kcal fat, and HFD was a cafeteria diet containing 60% kcal fat, were obtained from Arden Research and Experiment Company, Ankara, Turkey.

Probiotic capsule as Bifidobacterium infantis 35624 (Symbiosys Alflorex; Biocodex, France) was obtained from the local pharmacy in Ordu, Turkey. Each capsule contained 10⁹ Bifidobacterium infantis 35624 in powder form. The probiotic content was drawn into the syringe with 0.5 ml of water, diluted, and mixed for the supplementation therapy. Each rat in the HPFD group was fed daily with this probiotic supplementation by oral gavage.

The rat weights were recorded weekly. In the evaluation of obesity, the Body Mass Index (BMI = Body weight (g)/height (cm²)) value calculated by measuring the body weight and naso-anal length of the rats was used. BMI 0.48-0.68 g/cm² was determined as the normal range, and BMI > 0.68 g/cm² was evaluated as obese [9].

At the end of the 8-week treatment period, all rats were sacrificed by cervical dislocation under deep anesthesia. Intraperitoneal ketamine 90 mg/kg (Ketalar; Eczacıbaşı, Istanbul, Turkey) and xylazine hydrochloride 3 mg/kg (Rompun; Bayer, Leverkusen, Germany) were used for the anesthesia. All efforts were made to minimize suffering.

2.3. Biochemical Analysis

Blood samples were collected by entering the bifurcation aorta with a ten cc injector, and 4-5 ccs of blood was taken and transferred to appropriate laboratory parameter tubes with an empty glass. Glucose measurements were made using the colorimetric method. IL-6, TNF-α, GLP-1, and insulin levels were studied by ELISA (Sunred; Shanghai, China). All measurements were made in Ordu University Biochemistry Research Laboratory.

2.4. Statistical Analysis

Statistical analysis was performed using the Statistical Package for the Social Sciences software program, version 26.0 for windows. Power analysis was performed to determine the sample size using the G*Power 3.1.9.6 statistical program. The effect size was calculated with the help of the study conducted by Çelik and Söğüt [10] and found to be f = 0.6836. The total sample size calculated to reach 80% power value at a 95% confidence level was found to be 24. For this reason, the total sample size in the study was determined to be 24, with 8 rats in each group. All parametric data were described as the mean ± standard deviation. The significance of the differences in mean values among the two groups was evaluated by two-tailed unpaired Student's t tests. More than two groups were evaluated by a one-way ANOVA followed by Tukey's test. p value of <0.05 was considered significant.

3. Results

3.1. Body Weight, Glucose, and Insulin Levels

At the beginning of the study, the mean body weights of the groups were similar and BMI was 0.56 g/cm2 for each group. After eight weeks of the study, NFD group did not become obese (BMI: 0.60 g/cm²) while the HFD group was diagnosed with obesity (BMI:0.72 g/cm²). A significant difference in final body weight between the ND and HFD groups was observed (p<0.001). Moreover, the HPFD group showed a significantly lower mean body weight than the HFD group (p< 0.001). The weight and BMI values of HPFD group were similar to those of the NFD group. Plasma glucose and insulin levels were increased in the HFD group compared to the NFD group (p<0,004 and p<0.001 respectively). These metabolic parameters were significantly lower in the HPFD group than in the HFD group (p<0.005 and p<0.001 respectively). The comparison of the glucose and insulin levels was shown in Figures 1A and 1B.

3.2. Inflammatory Cytokines and Energy Metabolism Parameters

TNF-α and IL-6 levels increased in the HFD group compared to the NFD group (p<0.039 and p<0.017, respectively). However, these cytokines were significantly lower in the HPFD group than in the HFD group (p<0.031 and p<0.038, respectively). The TNF-α and IL-6 levels of the NFD group and HPFD group were found to be similar. The TNF-α and IL-6 levels of the groups were shown in Figure 2 and Figure 3.

GLP-1 levels increased in the HFD group compared to the NFD group (p<0,001). The GLP-1 levels were significantly lower in the HPFD group than in the HFD group (p<0.005). The GLP-1 levels in the NFD group and HPFD group were found to be similar. GLP-1 levels of the groups were shown in Figure 4. The morphometric and laboratory parameters evaluated in the study were shown in Table 1.

Figure 1A. The comparison of the glucose levels. NFD = Normal fat diet, HFD = High-fat diet, HPFD = High-fat diet with probiotic supplementation

Figure 1B. The comparison of the insulin levels. NFD = Normal fat diet, HFD = High-fat diet, HPFD = High-fat diet with probiotic supplementation

Figure 2. The comparison of the TNF- α levels. NFD = Normal fat diet, HFD = High-fat diet, HPFD = High-fat diet with probiotic supplementation

Figure 3. The comparison of the IL-6 levels. NFD = Normal fat diet, HFD = High-fat diet, HPFD = High-fat diet with probiotic supplementation

Figure 4. The comparison of the GLP-1 levels. NFD = Normal fat diet, HFD = High-fat diet, HPFD = High-fat diet with probiotic supplementation

Table 1. Morphometric and laboratory parameters of the study

4. Discussion

The alteration and function of the gut microbiota may lead to a pro-inflammatory state as the onset of some diseases and obesity [11]. Turnbaugh et al. compared gut microbiota composition in obese and lean individuals, and they reported that gut microbiota was different in both cases, suggesting that the alteration of the gut microbiota may be associated with an increased or reduced body weight [12]. The most commonly involved bacteria are Lactobacillus and Bifidobacterium in gut microbiota. Studies have shown that an imbalance between these species is the most common cause of the disorders in the human body [13]. Zuo et al. demonstrated that the major Bacteroidetes genus Bacteroides quantity was significantly lower in the obese group than in the normal-weight group as a result of the examination of the gut microbiota in obese and normal-weight individuals [14]. The changes in gut microbiota especially with the reduction of Bacteroidetes have been found to be associated with the obesity development in many studies [15]. In the present study, the weight gain in the HPFD group was significantly lower than that in the HFD group. Bifidobacterium infantis 35624 supplementation kept the weights similar to those of the normal diet feeding despite the high fat feeding. Likewise, plasma glucose and insulin levels were found to be significantly lower in the HPFD group than in the HFD group. Both energy metabolism imbalance and low-grade inflammation have been implicated in the pathophysiology of obesity and obesity-related diseases [16]. The main source of IL-6 and TNF-α is a macrophage infiltration of white adipose tissue (WAT) which induces insulin resistance in adipocytes [17]. Adipose tissue mass is largely formed by WAT which is mostly responsible for the triglycerides storage, and it is critical for energy storage, endocrine communication, and insulin sensitivity [18]. Increased adipose tissue in obesity causes an increase in the inflammatory cytokines IL-6 and TNF-α and a decrease in insulin sensitivity [19]. Adipose tissue contains the immune cells such as lymphocytes, monocytes, and macrophages. Increased adipose tissue and low grade inflammation are responsible for the release of the inflammatory cytokines IL-6 and TNF-α which were found to be related to the several disorders such as obesity, insulin resistance, and cardiovascular diseases. [20]. In the present study, obesity caused an increase in IL-6 and TNF-α levels. Similarly, in a recent study, the levels of pro-inflammatory cytokine IL-6 were found significantly higher in obese than non-obese participants [21]. Again in another study, the secretion of inflammatory cytokines and adipokines started while the secretion of anti-inflammatory and protective cytokines declined with the development of obesity [22]. It was stated that two main inflammatory processes work together to drive disease in the obesity status; the systemic low-grade inflammation that damages the vascular endothelium and causes organ dysfunction1, and a more aggressive adipose tissue inflammation that result to the release of cytokines such as IL-6 and TNF-α and adipokines and contributes to peripheral insulin resistance [23].

Food intake and energy balance are controlled via the gut microbiota, hormonal effects, and the nervous system. The gut influences the immune system with inflammatory responses to conditions such as infections, antibiotic treatments, vitamin deficiencies and some diseases throughout life. The gut microbiota plays an important role in these responses [24]. The end products of nutrients activate enteroendocrine cells (EECs) of the gut through the influence of gut bacteria. Nutrients are thus sensed by the paracrine effects of enterocytes [25]. Inflammation disrupts the control mechanism of the gut by damaging the intestinal epithelium, increasing the permeability of enterocytes and allowing some bacterial particles called lipopolysaccharide (LPS) to diffuse through the gut into the blood. Elevated levels of bacterial plasma LPS are known as "metabolic endotoxaemia" [26]. This status was found to be associated with obesity. LPS infusion was observed to increase total body weight, cause inflammation in adipose tissue, and induce fasting hyperglycaemia and hyperinsulinaemia [27]. In one study, a high-fat or high-carbohydrate meal was observed to induce this state [28]. In another study, experimental endotoxemia reduced systemic insulin sensitivity by 35% [29]. Metabolic endotoxemia was observed to be typically associated with a reduction in intestinal Bifidobacterium, which is known to maintain mucosal barrier function against bacterial antigens [30]. The gut plays an important role in maintaining energy balance and preventing obesity. Energy intake in the human body is controlled by GLP-1, a peptide hormone secreted by enteroendocrine cells [31]. After ingestion of a meal, the presence of nutrients in the intestinal lumen, and in particular ingested glucose and carbohydrates, stimulate GLP-1 secretion. The main function of GLP-1 is to stimulate pancreatic B-cells for insulin secretion and glucose uptake into peripheral tissue cells [32]. GLP-1, primarily produced by EECs following nutrient ingestion, is typically secreted within 10–15 min postprandially, peaking at 60–90 min. This effect is due to the release with the following oral glucose ingestion whereas intravenous glucose does not create this effect. This result shows that the intestinal mucosal cells and gut microbiota play an essential role in GLP-1 release [33]. The overweight and obese individuals had physiologically high levels of GLP-1, which has been shown to provide energy balance by increasing insulin activity [34]. Similarly, the present study found that insulin and GLP-1 levels were increased with a high-fat diet. This may be a response to increased food and calorie intake, as seen in other studies.

The gut microbiota has been found to be associated with GLP-1 secretion, and in the case of inflammation, the changes in the gut microbiota and impaired GLP-1 levels lead to insulin resistance and even diabetes mellitus [35]. Many studies have been indicated the beneficial effects of the probiotics in protecting the natural composition of the gut microbiota, preventing the metabolic endotoxemia and inflammation, reducing the inflammatory cytokines, and improving the GLP-1 secretion [36,37].

Some species of gut microbiota have been found to be more effective in improving obesity-related disorders. In particular, the knowledge that Bifidobacteria species decrease in obesity has led to a trend in research using these bacterial species as probiotics in this area [38]. In one study, Bifidobacterium spp probiotics improved glucose tolerance and insulin secretion. Moreover, the proinflammatory cytokines both in plasma and in adipose tissue changed in parallel with glucose and insulin levels [39]. In another study, the probiotic supplement used as an immunoregulator and containing Bifidobacterium pseudocatenulatum SPM 1204, Bifidobacterium longum SPM 1205 and Bifidobacterium longum SPM 1207 provided a reduction in adipose tissue and body weight with the lipid-lowering effect in obese rats induced by a high-fat diet [40]. Similarly, probiotic supplementation with Bifidobacterium spp. (including B. longum, B. bifidum, B. infantis and B. animalis) improved insulin resistance and reduced inflammatory adipocytokine expression in obese mice [41]. Bifidobacterium infantis strain 35624 is a naturally occurring microorganism in the gut. Its probiotic formula is well established in patients with functional gastrointestinal disorders and irritable bowel syndrome (IBS). TNF-α and IL-6 levels have been reduced in some intestinal and extra-intestinal inflammatory diseases by the use of Bifidobacterium infantis 35624, and it has been suggested that it modulates host inflammatory processes beyond the gut [42]. Similarly, in the present study, levels of the inflammatory cytokines IL-6 and TNF-α were found to be increased with high-fat feeding and decreased with Bifidobacterium infantis 35624 supplementation to levels close to those seen with normal-fat feeding.

5. Conclusions

The findings of this study are consistent with the view that pro-inflammatory cytokines TNF-α and IL-6 and indicator of energy metabolism GLP-1 increase with high-fat nutrition. As it is known that Bifidobacteria genus is a major part of the gut microbiota and some of its species have been found to have healing effects in obesity-related studies, Bifidobacterium infantis 35624 as probiotic may be also a candidate to be part of the therapeutic approach for the obesity prevention and treatment studies.

ACKNOWLEDGEMENTS

The authors would like to thank to Yeliz Kaşko Arıcı, Assistant Professor of Biostatistics Department of Medicine Faculty, Ordu University.

Author Contributions

All authors contributed to the study’s conception and design. Ö.Ö. was responsible for the conducting the search, screening potentially eligible studies and writing the reports. Ö.Ö. and Ç.A performed the experiments. Ç.A. and O.B. performed the sacrification and blood collection. In addition, Ç.A. was responsible for analyzing data, providing statistical analysis. F.E. contributed to design, review, and editing the study. T.B. performed laboratory analyzes and biochemical assessments.

Competing Interest

The authors declare that they have no competing interests.

Funding

This study was supported by Ordu University Scientific Project Coordination Department (ODUBAP, Project No: D-2204, 19/04/2022).

Data availability

Data is provided within the manuscript.

Consent for publication

Not applicable

References

[1]   | Caballero B. “Humans against Obesity: Who Will Win?” Adv Nutr,, 1;10. 4-9. Jan 2019.
[2]   | Saltiel, A.R, and Olefsky, J.M. “Inflammatory mechanisms linking obesity and metabolic disease.” J Clın Invest., 127, 1–4. 2017
[3]   | Drucker, D.J.,” Mechanisms of Action and Therapeutic Application of Glucagon-like Peptide-1.” Cell Metab., 3;27(4). 740-756. Apr 2018.
[4]   | Popko, K., Gorska. E, Stelmaszczyk-Emmel. A., Plywaczewski, R., Stoklosa, A., Gorecka, D., Pyrzak, B., and Demkow, U. “Proinflammatory cytokines IL-6 and TNF-α and the development of inflammation in obese subjects.” Eur J Med Res. 4;15(Suppl 2). 120-122. Nov 2010.
[5]   | Abenavoli, L., Scarpellini, E., Colica, C., Boccuto, L., Salehi, B., Sharifi-Rad, J. Aiello, V., Romano, B., De Lorenzo, A., Izzo, A.A., and Capasso, R.” Gut Microbiota and Obesity: A Role for Probiotics.” Nutrients., 7, 11(11). 2690. Nov 2019.
[6]   | Gomaa, E.Z., Human gut microbiota/microbiome in health and diseases: a review. Antonie Van Leeuwenhoek. 113(12). 2019-2040. Dec 2020.
[7]   | Amabebe, E., Robert, F.O., Agbalalah, T.,,and Orubu, E.S.F.” Microbial dysbiosis-induced obesity: role of gut microbiota in homoeostasis of energy metabolism.” Br J Nutr., 28;123(10). 1127-1137.May 2020.
[8]   | Yua, F., Ni, H., Asche, C.V., Kim, M., Walayat, S., and Ren, J. “Efficacy of Bifidobacterium infantis 35624 in patients with irritable bowel syndrome: a meta-analysis.” Curr Med Res Opın., 33(7).1191-1197. Jul 2017.
[9]   | Novelli, E.L.B., Diniz, Y.S., Galhardi, C.M., Ebaid, G.M.X., Rodrigues, H.G., Mani, F., Fernandes, A.A.H., Cicogna, A.C., and Filho, J.L.V.B. Anthropometrical parameters and markers of obesity in rats. Laboratory animals, 41(1). 111-119. Jan 2007.
[10]   | Çelik, M.N.,and Söğüt, M.Ü. Probiotics Improve Chemerin Levels and Metabolic Syndrome Parameters in Obese Rats. Balkan Med J., 22;36(5): 270-275. 2019.
[11]   | Dao, M.C., and Clément, K. Gut microbiota and obesity: concepts relevant to clinical care. Eur J Intern Med.; 48: 18–24. Feb 2018.
[12]   | Turnbaugh, P.J., Ley, R.E., Mahowald, M.A., Magrini, V., Mardis, E.R., and Gordon, J.I. An Obesity-Associated Gut Microbiome With Increased Capacity for Energy Harvest. Nature, 21; 444(7122). 1027–1031. Dec 2006.
[13]   | Boroni Moreira, A.P., Fiche Salles, Teixeira. T., Gouveia Peluzio, M.d.C., and Gonçalves Alfenas, R.d.C. Gut microbiota and the development of obesity. Nutr Hosp., 27(5). 1408-1414. Sep-Oct 2012.
[14]   | Zuo, H.J., Xie, Z.M., Zhang, W.W., Li, Y.R., Wang, W., Ding, X.B., and Pei, X.F. Gut bacteria alteration in obese people and its relationship with gene polymorphism. World J Gastroenterol., 28,17(8). 1076-1081. Feb 2011.
[15]   | Sun, L., Ma, L., Ma, Y., Zhang, F., Zhao, C., and Nie, Y. Insights into the role of gut microbiota in obesity: pathogenesis, mechanisms, and therapeutic perspectives. Protein Cell, 9(5). 397–403. May 2018.
[16]   | Stolarczyk, E. Adipose tissue inflammation in obesity: a metabolic or immune response? Curr Opin Pharmacol., 37. 35-40. Dec 2017.
[17]   | Kern, P.A., Ranganathan, S., Li, C., and Wood, L. Ranganathan G. Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. Am J Physiol Endocrinol Metab., 280(5). 745-751. May 2001.
[18]   | Bagchi, D.P., and MacDougald, O.A. Identification and Dissection of Diverse Mouse Adipose Depots. J Vis Exp.,.11:(149):10.3791/59499. Jul 2019.
[19]   | Fain, J.N. Release of inflammatory mediators by human adipose tissue is enhanced in obesity and primarily by the nonfat cells: A review. Mediators Inflamm., 2010. 513948. 2010.
[20]   | Moghbeli, M., Khedmatgozar, H., Yadegari, M., Avan, A., Ferns, G.A., and Mobarhan, M.G. Cytokines and the immune response in obesity-related disorders. Adv Clin Chem., 101, 135-168. 2021
[21]   | Khathlan NA. Association of inflammatory cytokines with obesity and pulmonary function testing. PLoS One, 22;18(11):e0294592. Nov 2023.
[22]   | Stanek, A., Brożyna-Tkaczyk, K., and Myśliński,,W. The role of obesity-induced perivascular adipose tissue dysfunction in vascular homeostasis. Nutrients. 28;13(11):3843. Oct 2021.
[23]   | Soták, M., Clark, M., Suur,  B.E., and Börgeson, E. Inflammation and resolution in obesity. Nat Rev Endocrinol., 21(1):45-61. Jan 2025.
[24]   | Steinerta, A., Radulovicc, K., and Niess, J.H. Gastrointestinal tract: the leading role of mucosalimmunity. Swiss Med Wkly., 5:146:w14293. Apr 2016.
[25]   | Tilg, H., and Kaser, A. Gut microbiome, obesity, and metabolic dysfunction. J Clın Inves., 121: 2126-2132. Jun 2011.
[26]   | Mohammad, S., and Thiemermann, C. Role of Metabolic Endotoxemia in Systemic Inflammation and Potential Interventions. Front Immunol., 11: 594150. Jan 2021.
[27]   | Cani, P.D., Delzenne, N.M., Amar, J., and Burcelin, R.. Role of gut microflora in the development of obesity and insulin resistance following high-fat diet feding. Pathol Biol (Paris). 56(5):305-309. Jul 2008.
[28]   | Amar, J., Burcelin, R., Ruidavets, J.B., Cani, P.D, Fauvel, J., Alessi, M.C., Chamontin, B.., and Ferriéres, J. Energy intake is associated with endotoxemia in apparently healthy men. Am J Clin Nutr.; 87(5): 1219-1223. May 2008.
[29]   | Mehta, N.N., McGillicuddy, F.C., Anderson, P.D., Hinkle, C.C., Shah, R., Pruscino, L., Tabita-Martinez, J., Sellers, K.F., Rickels, M.R., and Reilly, M.P. Experimental endotoxemia induces adipose inflammation and insulin resistance in humans. Diabetes., 59: 172-181. Jan 2010.

[30]  
Cani, P.D., Neyrinck, A.M., Fava, F., Knauf, C., Burcelin, R.G., Tuohy, K.M., Gibson, G..R., and Delzenne, N.E. Selective increases of bifidobacteria in gut microflora improves high-fat diet induced diabetes in mice through a mechanism associated with endotoxemia. Diabetologia., 50(11): 2374–2383. Nov 2007.

[31]   | Hira, T., Pinyo, J., and Hara, H. What Is GLP-1 Really Doing in Obesity? Trends Endocrın Met., 31(2): 71-80. Feb 2020.
[32]   | Cho, Y.M., Fujita, Y., and Kieffer, T.J. Glucagon-like peptide-1: glucose homeostasis and beyond. Annu Rev Physıol.; 76: 535-559. 2014.
[33]   | Chen, Q., Gao, Y., Li, F., and Yuan, L. The role of gut–islet axis in pancreatic islet function and glucose homeostasis. Diabetes Obes Metab., 27(4):1676-1692. Apr 2025.
[34]   | Adam, T.C., Jocken, J., and Westerterp-Plantenga, M.S. Decreased glucagon-like peptide 1 release after weight loss in overweight/obese subjects. Obes Res. 13(4): 710-716. Apr 2005.
[35]   | Muscogiuri, G., Balercia, G., Barrea, L., Cignarelli, A., Giorgino, F., Holst, J.J, Laudisio, D., Orio, F., Tirabassi, G., and Colao, A. Gut: A key player in the pathogenesis of type 2 diabetes? Crit Rev Food Sci Nutr., 24: 1294-1309. May 2018.
[36]   | Cerdó, T., García-Santos, J.A., Bermúdez, M.G., and Campoy, C. The Role of Probiotics and Prebiotics in the Prevention and Treatment of Obesity. Nutrients., 15, 11(3): 635-666. Mar 2019.
[37]   | Saadati, S., Naseri, K., Asbaghi, O., Yousefi, M., Golalipour, E., and De Courten, B. Beneficial effects of the probiotics and synbiotics supplementation on anthropometric indices and body composition in adults: A systematic review and meta-analysis. Obes Rev., 25(3):e13667. Mar 2024
[38]   | Mazloom, K., Siddiqi, I., and Covasa, M. Probiotics: How Effective Are They in the Fight against Obesity? Nutrients., 24;11(2):258. Jan 2019.
[39]   | Di Gioia, D., Aloisio, I., Mazzola, G., and Biavati, B. Bifidobacteria: their impact on gut microbiota composition and their applications as probiotics in infants. Applied Microbiology and Biotechnology, 98(2). 563–577.Jan 2014.
[40]   | An, H.M., Park, S.Y., Lee, D.K., Kim, J.R., Cha, M.K., Lee, S.W., Lim, H.T., Kim, K.J., and Ha, N.J. Antiobesity and lipid-lowering effects of Bifidobacterium spp. in high fat diet-induced obese rats. Lipids Health Dis., 10: 116. Jul 2011.
[41]   | Chung LE, T.K., Hosaka, T., Tam Le, T.T., Nguyen, T.G., Tran, Q.B., Hao Le, T.H., and Da Pham, X. Oral administration of Bifidobacterium spp. improves insulin resistance, induces adiponectin, and prevents inflammatory adipokine expressions. Biomed Res., 35(5). 303-310. 2014.
[42]   | Groeger, D., O’Mahony, L., Murphy, E.F., Bourke, J.F., Dinan, T.G., Kiely, B., Shanahan, F.,and M Quigley, F. Bifidobacterium infantis 35624 modulates host inflammatory processes beyond the gut. Gut Microbes, 4(4). 325-339. 2013