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Probiotics, Prebiotics, and Gut Health: New Frontiers in Treating Obesity, Diabetes, and Metabolic Disorders

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Diabetes".

Deadline for manuscript submissions: closed (25 March 2026) | Viewed by 3659

Special Issue Editor

Prof. Dr. Kequan Zhou

E-Mail Website
Guest Editor
Department of Nutrition and Food Science, Wayne State University, Detroit, MI 48202, USA
Interests: nutraceutical and functional food; bioactive food components; probiotics; chronic diseases; type 2 diabetes; obesity

Special Issue Information

Dear Colleagues,

The objective of this Special Issue is to explore the intricate connection between the gut microbiome and metabolic health, specifically focusing on the therapeutic potential of probiotics and prebiotics. We aim to provide a comprehensive overview of how modulating gut microbiota can influence the prevention and management of a wide range of chronic metabolic diseases, including obesity, type-2 diabetes, and related conditions.

Topics of interest include, but are not limited to, the following:

  • The impact of dietary fibers and beneficial microbial strains on body weight regulation and fat metabolism.
  • The role of gut microbiota-derived metabolites (e.g., short-chain fatty acids) in influencing insulin sensitivity, glucose metabolism, and appetite regulation.
  • How gut barrier integrity, systemic inflammation, and immune function are modulated by prebiotics and probiotics.
  • Clinical studies and mechanistic research examining the efficacy of microbial interventions in managing obesity and diabetes.
  • The influence of the gut–brain axis on metabolic health and energy homeostasis.

The Special Issue seeks to synthesize recent advancements, highlighting promising clinical applications and identifying key areas for future research at the intersection of gut health and chronic disease.

Prof. Dr. Kequan Zhou
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diabetes
  • prebiotics
  • probiotics
  • synbiotics
  • glycemic control
  • insulin resistance
  • inflammation
  • gut microbiome
  • gut barrier integrity
  • microbiota-targeted therapies

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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19 pages, 719 KB  
Article
Severity of Hypoxia-Induced Effects on 3T3-L1 Adipocyte Secretory Function Is Attenuated Dose-Dependently by Individual Short-Chain Fatty Acids
by Jessie L. Burns, Kelsey Van, Ala Alzubi, Clara E. Cho and Jennifer M. Monk
Nutrients 2026, 18(6), 942; https://doi.org/10.3390/nu18060942 - 17 Mar 2026
Viewed by 604
Abstract
Background: Microbial fermentation of non-digestible carbohydrates and proteins produce short-chain fatty acids (SCFAs), which are critical communication signals in the gut–adipose tissue axis. Individual SCFA can differentially modulate the adipocyte secretory profile and adipose tissue metabolic function; however, their dose-dependent effects on [...] Read more.
Background: Microbial fermentation of non-digestible carbohydrates and proteins produce short-chain fatty acids (SCFAs), which are critical communication signals in the gut–adipose tissue axis. Individual SCFA can differentially modulate the adipocyte secretory profile and adipose tissue metabolic function; however, their dose-dependent effects on adipocyte function in combined inflammatory and hypoxic environmental conditions that reflect the obesity-associated adipose tissue phenotype remain unknown. Methods: Mature 3T3-L1 adipocytes were cultured for 24 h with lipopolysaccharide (LPS; 10 ng/mL) plus 100 µM of cobalt chloride (CoCl2) to chemically induce hypoxia ± individual SCFAs, namely acetate (Ace), propionate (Pro), and butyrate (But), in a dose-dependent manner (0.25 mM, 0.5 mM, and 1 mM). Results: Ace, Pro and But reduced secretion of IL-6, MCP-1/CCL7 and Rantes/CCL5 in a dose-dependent manner, whereas Pro and But reduced MCP3/CCL7 secretion and only But reduced resistin and increased adiponectin secretion compared to control (p < 0.05). Intracellular protein expression of the ratio of phosphorylated–to–total NFκB p65 was reduced by 1 mM But, whereas the ratio of phosphorylated–to–total STAT3 expression was reduced by 1 mM Ace, Pro and But and 0.5 mM Pro and But compared to control (p < 0.05). There was no difference in insulin-stimulated or non-insulin-stimulated glucose uptake between control and any individual SCFAs (p > 0.05). Conclusions: Adipocyte adipokine secretory function in combined inflammation and hypoxic environmental conditions is dose-dependently attenuated by individual SCFA, which exhibit both individual and overlapping effects. Full article
(This article belongs to the Special Issue Probiotics, Prebiotics, and Gut Health: New Frontiers in Treating Obesity, Diabetes, and Metabolic Disorders)
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15 pages, 2491 KB  
Article
C. cochlearium 2316 Ameliorates High-Fat Diet-Induced Obesity and Metabolic Syndrome Risk Factors via Enhanced Energy Expenditure and Glucose Homeostasis
by Wenjun Zhu, Paba Edirisuriya, Qing Ai, Fei Yang, Jiangqi Tang, Kai Nie, Xiangming Ji, Samira Soltanieh, Maesha Musarrat, Md Abdul Alim, Zerui Liao and Kequan Zhou
Nutrients 2025, 17(24), 3848; https://doi.org/10.3390/nu17243848 - 10 Dec 2025
Viewed by 612
Abstract
Objectives: This study investigated the potential beneficial effects of a probiotic candidate, Clostridium cochlearium 2316, in modulating physiological and metabolic markers in mice with high-fat diet-induced obesity (DIO). Methods: C57BL/6 DIO mice were assigned to three groups (ad libitum): standard low-fat control (LF, [...] Read more.
Objectives: This study investigated the potential beneficial effects of a probiotic candidate, Clostridium cochlearium 2316, in modulating physiological and metabolic markers in mice with high-fat diet-induced obesity (DIO). Methods: C57BL/6 DIO mice were assigned to three groups (ad libitum): standard low-fat control (LF, 10% fat), high-fat diet (HF, 60% fat), and high-fat diet supplemented with approximately one billion CFU/day of CC2316 via daily oral gavage for 16 weeks. Results: After 16 weeks, the CC group exhibited 17.3% lower body weight gain (p < 0.001) and significant fat mass decrease (p < 0.0001) compared to HF mice. Serum biochemistry showed that CC2316 supplementation resulted in a 27.7% reduction in fasting blood glucose (p < 0.05), a 58.4% reduction in fasting insulin (p < 0.01), and an 89.4% improvement in HOMA-IR score (p < 0.05). Furthermore, serum total cholesterol level decreased dramatically by 40.2% in the CC group (p < 0.001). Despite a higher caloric absorption rate (p < 0.001), CC mice demonstrated a significant beneficial shift in energy expenditure, characterized by an increased basal metabolic rate (p < 0.05), higher energy expenditure (p < 0.05), and an elevated respiratory quotient (RER) (p < 0.05), alongside increased physical activity (p < 0.05). Conclusions: This investigation strongly suggests that CC2316 supplementation mitigates the adverse effects of HFD-induced obesity by modulating whole-body energy metabolism, positioning it as a potential aid to lower risk factors associated with metabolic syndrome. The precise mechanisms linking the gut microbiome to altered energy substrate utilization are discussed and suggested for further investigation. Full article
(This article belongs to the Special Issue Probiotics, Prebiotics, and Gut Health: New Frontiers in Treating Obesity, Diabetes, and Metabolic Disorders)
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Review

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22 pages, 907 KB  
Review
Oral–Gut Microbiota Crosstalk and Epigenetic Targets in Metabolic and Neuropsychiatric Diseases
by Sahar Mostafavi, Shabnam Nohesara, Ahmad Pirani, Hamid Mostafavi Abdolmaleky and Sam Thiagalingam
Nutrients 2025, 17(21), 3367; https://doi.org/10.3390/nu17213367 - 27 Oct 2025
Cited by 1 | Viewed by 1878
Abstract
The oral cavity contains a diverse group of bacteria in the saliva, as well as structured aggregates of bacterial cells on the mucosal surfaces. Oral microbiota (OM) dysbiosis not only induces local inflammation, it can also trigger systemic inflammation leading to metabolic diseases [...] Read more.
The oral cavity contains a diverse group of bacteria in the saliva, as well as structured aggregates of bacterial cells on the mucosal surfaces. Oral microbiota (OM) dysbiosis not only induces local inflammation, it can also trigger systemic inflammation leading to metabolic diseases and neuropsychiatric diseases (NPDs). While primary evidence indicates that oral microbiota dysbiosis induces gut microbiota aberrations, which exacerbate inflammation associated with metabolic diseases (obesity, dyslipidemia, diabetes, nonalcoholic fatty liver disease (NAFLD), and insulin resistance), other studies revealed the contribution of the oral microbiota–brain axis in the pathogenesis of NPDs. GM dysbiosis and inflammation also induce epigenetic alterations in cytokine genes, such as IL-1β, IL-6, TNF-α, NF-kB, BTLA, IL-18R1, TGF-β, P13k/Akt1, Ctnnb1, and Hsp90aa1, as well as DNMTs, HDACs, and DAT1 associated with the development and progression of metabolic disorders and/or NPDs. Therefore, the epigenome could serve as a target for preventive or therapeutic interventions. Here, we (i) review emerging evidence of the potential impact of OM dysbiosis in the pathogenesis of metabolic diseases and NPDs, (ii) highlight the relationship between OM-induced inflammation and epigenetic alterations driving NPDs pathogenesis and interlinked metabolic aberrations, (iii) discuss therapeutic approaches capable of treating metabolic diseases and NPDs through reshaping the microbiota and its epigenetic metabolites, and hence mitigating epigenetic aberrations linked to metabolic diseases and NPDs. Finally, we outline challenges and current research gaps related to investigating the relationship between microbiota, epigenetic aberrations, and metabolic abnormalities associated with NPDs. Full article
(This article belongs to the Special Issue Probiotics, Prebiotics, and Gut Health: New Frontiers in Treating Obesity, Diabetes, and Metabolic Disorders)
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