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Wang, C.; Yi, Z.; Jiao, Y.; Shen, Z.; Yang, F.; Zhu, S. Gut Microbiota and Adipose Tissue Microenvironment in Obesity. Encyclopedia. Available online: (accessed on 13 June 2024).
Wang C, Yi Z, Jiao Y, Shen Z, Yang F, Zhu S. Gut Microbiota and Adipose Tissue Microenvironment in Obesity. Encyclopedia. Available at: Accessed June 13, 2024.
Wang, Congcong, Zihan Yi, Ye Jiao, Zhong Shen, Fei Yang, Shankuan Zhu. "Gut Microbiota and Adipose Tissue Microenvironment in Obesity" Encyclopedia, (accessed June 13, 2024).
Wang, C., Yi, Z., Jiao, Y., Shen, Z., Yang, F., & Zhu, S. (2023, July 14). Gut Microbiota and Adipose Tissue Microenvironment in Obesity. In Encyclopedia.
Wang, Congcong, et al. "Gut Microbiota and Adipose Tissue Microenvironment in Obesity." Encyclopedia. Web. 14 July, 2023.
Gut Microbiota and Adipose Tissue Microenvironment in Obesity

Obesity is an increasingly serious global health problem. Some studies have revealed that the gut microbiota and its metabolites make important contributions to the onset of obesity. The gut microbiota is a dynamic ecosystem composed of diverse microbial communities with key regulatory functions in host metabolism and energy balance. Disruption of the gut microbiota can result in obesity, a chronic metabolic condition characterized by the excessive accumulation of adipose tissue. Host tissues (e.g., adipose, intestinal epithelial, and muscle tissues) can modulate the gut microbiota via microenvironmental interactions that involve hormone and cytokine secretion, changes in nutrient availability, and modifications of the gut environment. The interactions between host tissues and the gut microbiota are complex and bidirectional, with important effects on host health and obesity.

gut microbiota metabolites adipose tissue microenvironment obesity

1. Introduction

Obesity, a widespread public health problem, has serious negative effects on quality of life and well-being worldwide. According to the World Health Organization, obesity rates have doubled since 1975, such that it currently affects more than 650 million adults globally [1]. This alarming trend is attributed to numerous factors, including changes in dietary habits and physical activity levels, as well as sedentary lifestyles; thus, it constitutes a primary public health concern in many countries.
The gut microbiota, a large community containing trillions of bacteria, viruses, and other microorganisms, plays a key role in the progression of obesity [2]. There is substantial evidence regarding its essential roles in energy regulation, whereby it facilitates nutrient uptake, metabolism, and storage [3]. Moreover, inherent dysbiosis within the gut microbiota has been implicated in the pathogenesis of obesity and associated metabolic morbidities [4].

2. The Association between the Gut Microbiota and Obesity

There is considerable evidence of a strong association between obesity and the gut microbiota; significant changes in gut microbiota composition have been observed in obese individuals. Table 1 provides an overview of the common obesity-related changes in microbiota [5][6][7]. Several animal and human studies have demonstrated microbial changes in obesity condition. For example, Turnbaugh et al. [2] compared obese and lean individuals in mice and human volunteers and observed a reduction in Bacteroidetes and a proportional increase in Firmicutes in the obese group. They suggested that the obese microbiome has an increased capacity to harvest energy from the diet and that this trait was transmissible, indicating that the gut microbiota is an additional contributing factor to the pathophysiology of obesity.
Table 1. Obesity-associated changes in the gut microbiota.
Upregulated Downregulated Reference
Firmicutes to Bacteroidetes ratio
Bacteroidetes; Turnbaugh PJ et al., Nature. (2006) [2];
Hildebrandt MA et al., Gastroenterology. (2009) [8]
Clostridium cluster XIVa Lactobacillus;
Clostridium cluster IV;
Faecalibacterium prausnitzii;
Remely M et al., Benef Microbes. (2015) [9]
Mollicutes Akkermansia;
Thingholm LB et al., Cell Host Microbe. (2019) [7]
Escherichia-Shigella Faecalibacterium Anhê FF et al., Nat Metab. (2020) [6]
Furet JP et al., Diabetes. (2010) [10]
  Oscillospira Gophna U et al., Environ Microbiol. (2017) [11]
  Bacteroides thetaiotaomicron Liu R et al., Nat Med. (2017) [5]
  de La Serre CB et al., Am J Physiol Gastrointest Liver Physiol. (2010) [12]
Desulfovibrionaceae   Zhang C et al., ISME J. (2010) [13]
Fibrobacteres   Geurts L et al., Front Microbiol. (2011) [14]
Changes in gut microbiota composition and functionality have been implicated in the onset and progression of obesity via modulation of energy metabolism, insulin sensitivity, and inflammatory signaling pathways [15].

3. Gut Microbiota-Derived Metabolites Associated with Obesity

3.1. Bile Acids

Bile acids, a class of steroid compounds, are synthesized in the liver and stored in the gallbladder. Upon food intake, these molecules are released into the small intestine where they play important roles in the digestion and absorption of dietary fat, as well as fat-soluble vitamins. Bile acids also function as signaling molecules, with key contributions to systemic metabolic maintenance. These contributions are facilitated by their interactions with various nuclear receptors, including (but not limited to) the farnesoid X receptor [16], vitamin D receptor [17], pregnane X receptor [18], and androstane receptor [19], as well as membrane receptors (e.g., Takeda G protein-coupled receptor 5 [20]). These interactions regulate the secretion of key factors such as peptide YY (PYY), glucagon-like peptide-1 (GLP-1), and fibroblast growth factor 19 (FGF19); they also influence cholesterol metabolism and systemic energy expenditure [21].
Bile acids function as substrates for biotransformation by the gut microbiota, thereby influencing the composition and behavior of the microbial community within the gastrointestinal lumen. For example, the microbiota promotes biosynthesis of secondary bile acids [22][23], including deoxycholic acid and lithocholic acid.
The metabolism of the gut microbiota affects both the bioavailability and bioactivity of bile acids; these properties influence the metabolic processes in which bile acids participate, as well as the development of obesity [24]. Studies in animal models have demonstrated that gut microbiota-mediated regulation of bile acid synthesis and metabolism can influence body weight and fat distribution; the inhibition of bile acid synthesis leads to improved glucose tolerance [25] and weight loss [26]

3.2. SCFAs

Short-chain fatty acids (SCFAs) are produced in the gastrointestinal tract via microbial fermentation of carbohydrates; acetate, propionate, and butyrate are the primary SCFAs produced by this method [27]. The production of SCFAs is influenced by changes in gut microbiota structure and function; a decrease in the number of butyrate-producing bacteria is closely associated with increased energy storage and weight gain in both animal models and humans [28]. Butyrate regulates energy metabolism by interacting with various metabolic pathways; it can stimulate energy expenditure while mitigating adipocyte size via lipogenesis inhibition and the promotion of lipolysis-related genes [29].
SCFAs provide energy for the epithelial cells and influence the immune function of the mucosa, by regulating the pH and the production of mucus in the intestinal lumen. Increased mucus production is usually inferred from increased expression of the MUC2 gene encoding mucin 2, and SCFAs, particularly butyrate, stimulate MUC2 gene expression through selective acetylation/methylation of the MUC2 histone, thereby promoting mucus production [30].
SCFAs regulate appetite and food intake by influencing communication between the gastrointestinal tract and the central nervous system [30][31][32][33]. One of these mechanisms involves the stimulation of colonic cells that express free fatty acid receptor 2 (FFAR2) and free fatty acid receptor 3 (FFAR3) [34], which are receptors for SCFAs, especially acetate and propionate. Upon activation, these cells secrete hormones that promote satiety, such as PYY and GLP-1.

3.3. Amino Acids

The gut microbiota is a major source of various metabolites, including amino acids. The diverse effects of these compounds on energy balance and metabolic homeostasis are mediated by multiple mechanisms. For example, gut microbiota-derived amino acids have been consistently implicated in alterations of energy metabolism, regulation of body weight, and accumulation of adipose tissue. Notably, phenylalanine is converted to tyrosine, which serves as a precursor to catecholamines such as epinephrine and norepinephrine. By enhancing energy expenditure, promoting fat oxidation, and activating brown adipose tissue, these catecholaminergic molecules may contribute to obesity prevention [35].
Tryptophan, an essential amino acid, is utilized in protein synthesis; it also plays a key role in the gut microbiota-mediated regulation of body weight and metabolism [36]. Tryptophan and its metabolites can transmit signals locally, especially in the intestinal mucosa; they can also transmit signals to other organs, such as the brain [37]. Some tryptophan metabolites, which are derived from microbial degradation, have demonstrated robust effects on appetite regulation in various experimental models [38][39][40]. These metabolites include tryptamine, indole-3-acetic acid, and 3-indole-propionic acid, all of which serve as ligands for the aryl hydrocarbon receptor (AhR), a naturally occurring receptor for aryl hydrocarbons [41]. AhR, a sensor for environmental and physiological signals, has strong effects on intestinal barrier function, immune response, and metabolism [42][43]. Altered levels of tryptophan-derived metabolites have been detected in stool samples from individuals with metabolic syndrome; these changes were associated with reduced AhR activity [41].

3.4. Other Gut Microbiota-Derived Metabolites

Extensive research concerning the roles of gut microbiota-derived metabolites in obesity has been performed [44][45][46]. Some of these metabolites include phenolic acids, lipopolysaccharides, ethanol, and microbial-derived protein fermentation products. These metabolites contribute to obesity by affecting insulin sensitivity, altering energy balance, and causing low-grade inflammation. For example, phenolic acids can modulate adipocyte differentiation and lipolysis [45], lipopolysaccharides can induce inflammation and impair glucose uptake in adipose tissue, ethanol can increase hepatic lipid accumulation and insulin resistance [45], and protein fermentation products can activate pro-inflammatory pathways and reduce energy expenditure [45].

4. Microbiota–Target Tissue Interactions in Obesity

4.1. Adipose Tissue

Obesity is primarily characterized by irregularities in adipose tissue, which mainly comprise atypical fat distribution and adipose tissue dysfunction. Abnormal fat distribution is defined as excessive accumulation of visceral adipose tissue in the intraperitoneal and retroperitoneal regions, as well as ectopic fat deposition in non-physiological sites (e.g., liver, pancreas, heart, and skeletal muscle). Adipose tissue dysfunction involves impaired adipogenesis, adipocyte hypertrophy, and anomalous lipid metabolism [47]. The pathogenesis underlying adipose tissue dysfunction is related to the perpetuation of a vicious cycle [48] characterized by macrophage infiltration and proinflammatory polarization (M1 polarization), which triggers a cascade of inflammatory pathways that have detrimental effects on insulin signaling [49].
The interaction of specific dietary factors, such as a high-fat diet and certain gut microbiota, can interfere with adipose tissue function and lead to severe adipose tissue dysfunction [50]. Tran et al. showed that Western diet-induced dysbiosis can cause adipose tissue inflammation in mice, as demonstrated by an increase in typical proinflammatory M1 macrophages and a decrease in anti-inflammatory M2 macrophages within adipose tissue [51]. They also showed that the ablation of gut microbiota could reduce this inflammatory response within adipose tissue. Additionally, experimental knockdown of the Toll-like receptor (TLR) signaling protein myeloid differentiation primary response protein 88 (MyD88) yielded a phenotype similar to the phenotype caused by microbiota ablation, supporting the notion that Western diet-induced adipose tissue inflammation does not result from lipid accumulation; instead, the microbiota and/or its metabolites activate innate immune signaling pathways, which lead to inflammation.
Additionally, the results of recent studies are consistent with the notion that gut microbiota dysbiosis represents an early indication of inflammation and obesity [52]. The gastrointestinal system interacts with the dietary components involved, which disrupts the gut microbiota’s balance and alters the secretion profiles of gut peptides [12]. These disruptions trigger an inflammatory response in the intestinal mucosa, causing damage to the epithelial barrier and enhancing LPS entry into the systemic circulation. LPS and saturated fatty acids can activate TLRs, which are receptors that recognize microbial molecules, on macrophages or intestinal epithelial cells [53]. This leads to low-grade systemic inflammation. TLRs are also expressed in adipose tissue, where they can be activated by LPS and induce the secretion of inflammatory cytokines, such as TNF-α, IL-6, IL-8, and MCP-1, by macrophages and adipocytes [54][55][56][57]. These cytokines can attract more inflammatory cells to adipose tissue and worsen the inflammation. Chronic inflammation can also affect the gut microbiota and cause dysbiosis [58].

4.2. Intestinal Epithelium

Gut barrier dysfunction and gut microbiota dysbiosis are linked to a diverse array of pathological conditions, including obesity, T2DM, and inflammatory bowel disease. Intestinal epithelial cells play a key role in maintaining the health of the gut microbiota. These cells form a physical barrier between the gut microbiota and the underlying tissues, preventing the migration of harmful bacteria and small molecules into the systemic circulation. Tight junctions between the epithelial cells function as gatekeepers that regulate the entry of nutrients and other substances into the intestinal epithelium. Dysregulation involving these junctions can lead to gut dysbiosis and intestinal permeability, triggering various pathological conditions.The Firmicutes phylum, including the Lactobacillus genus, has been linked to obesity and T2DM [59]. However, some genera in this phylum (e.g., Lactobacillus paracasei and Lactobacillus plantarum) can help to prevent weight gain [60][61]. Decreased relative abundances of Bacteroides and Bifidobacterium, as well as the butyrate-producing Faecalibacterium prausnitzii and Roseburia intestinalis, have been associated with obesity [62][63][64]. In T2DM patients, bariatric surgery increases the relative abundance of F. prausnitzii while improving glucose homeostasis, low-grade inflammation, and intestinal epithelial permeability [10][65]. F. prausnitzii is a key producer of butyrate, which serves as an important energy source for intestinal epithelial cells [66]. Multiple butyrate-mediated mechanisms (e.g., mucin synthesis [67], reorganization of tight junctions, and upregulation of occludin and Zonula occludens protein 1 [68][69]) can reduce local inflammation and improve intestinal barrier permeability. The species Bacteroides vulgatus and Bacteroides dorei may provide benefits for T2DM patients by increasing Zonula occludens protein 1 (ZO-1) expression and enhancing epithelial barrier function [70]. These bacteria produce bacteriocins, a class of proteins that inhibit the growth of specific microbes and could reduce the abundance of harmful species [71]

4.3. Muscle

Skeletal muscle, which comprises approximately 40% of the human body mass, is responsible for numerous critical functions including thermoregulation and the modulation of glucose/amino acid metabolism. Although it is physically distinct from the gut, skeletal muscle is influenced by gut-derived signals that arise from interactions between gut microbiota and host tissue; these interactions involve microbes, metabolites, gut peptides, LPS, and ILs. These signals form a link between gut microbiota activity and skeletal muscle function; modulation of these signals influences systemic or tissue inflammation and insulin sensitivity, helping to regulate muscle function. Disruptions in gut microbiota composition can lead to muscle atrophy, weakness, and poor exercise performance. Additionally, some microbial metabolites, such as SCFAs, have direct effects on muscle health and function, highlighting the complex interactions between gut microbiota and muscle physiology. Thus, the gut microbiota represents a promising new target for the prevention and treatment of muscle-related diseases.
Considering the diverse array of gut microbiota-derived metabolites, research has focused on the potential for SCFAs to mediate interactions among the gut microbiota, gastrointestinal physiology, and muscle insulin sensitivity. Comparative analyses have revealed that exercise interventions are associated with greater abundances of SCFA-producing microbial taxa, compared with the abundances in individuals with sarcopenia. SCFAs are primarily generated by microbial anaerobic fermentation of nondigestible dietary fibers, mainly within the distal ileum and colon. Acetate, propionate, and butyrate comprise the predominant SCFA profile within the colon, totaling more than 95% of the total SCFA content. Upon entry into enterocytes, butyrate drives the citric acid cycle through acetyl-CoA, satisfying up to 60–70% of colonocyte metabolic needs [28]. The remaining SCFAs are transported through the portal vein to the liver, which absorbs up to 80% of the available propionate and 40% of the available acetate for subsequent utilization in gluconeogenesis [28][72]. Finally, a small subset of SCFAs, predominantly acetate, is transported to skeletal muscle.
SCFAs are important for maintaining glucose and lipid homeostasis, regulating inflammation, and establishing connections between the gut and distant tissues [28][73]. There is empirical evidence that SCFA supplementation can enhance muscle mass and strength, particularly in germ-free and antibiotic-treated rodents [74][75][76][77]. Notably, acetate supplementation (via dietary intake or subcutaneous injection) enhances glucose uptake and glycogen content while reducing lipid accumulation in rat skeletal muscles [78]

5. Conclusions

The cumulative findings of numerous studies highlight the complex and multifaceted link between intestinal microflora and obesity. These studies have demonstrated that gut microbiota dysregulation influences energy equilibrium and can contribute to the onset of obesity. Furthermore, these studies have identified potential mechanisms by which the gut microbiota and its metabolites affect the onset of obesity, including the production of endogenous metabolites, regulation of systemic inflammation, and modulation of the adipose tissue microenvironment.


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