Second, people with less bacterial diversity in their gut had a higher proportion of visceral fat—confirming, in other words, the finding that obesity is correlated with having less diverse gut bacteria. But a study in mice hints that it might be the case.

In that study, researchers bred mice in bacteria-free environments. Then one mouse got gut bacteria implanted from those of an obese woman, while the other mouse got bacteria from her lean twin sister.

Even though the mice were fed the exact same diet, the first mouse became obese while the other remained lean. The most promising treatment would be fecal transplants , to populate their guts with bacteria from lean people. Trials of such treatments have run into some problems recently.

But with obesity at epidemic proportions in a growing number of countries, it may be a technique worth pursuing. Our free, fast, and fun briefing on the global economy, delivered every weekday morning. The A. Club Deadspin Gizmodo Jalopnik Kotaku Quartz The Root The Takeout The Onion The Inventory.

Support Quartz Journalism Support Us. Search Free Newsletters. King's College London provides funding as a member of The Conversation UK. Public health policy has mainly focused on diet to reverse these rising rates, but the impact of these policies has been limited.

The latest science suggests why this strategy is failing: one diet does not fit all. Dietary advice needs to be personalised. The reason one diet does not suit all may be found in our guts.

Our previous research showed that microbes in the digestive track, known as the gut microbiota, are linked to the accumulation of belly fat. Our gut microbiota is mostly determined by what we eat, our lifestyle and our health. So it is difficult to know exactly how food and gut microbes together influence fat accumulation and ultimately disease risk.

Our latest study provides new insights into these interactions. Animal studies have been valuable in showing that gut microbes alone can reduce the build-up of fat , resulting in better health. But translating these findings to humans is difficult, especially considering that we can eat very different foods.

In our study, we aimed to disentangle the effect of gut microbes and diet on the accumulation of belly fat in 1, twins from the UK. We found that the composition of the gut microbiota predicts belly fat more accurately than diet alone.

We identified a few specific nutrients and microbes that were bad for us and linked to an increase in belly fat, as well as a few nutrients and many microbes that were good for us and linked to reduced belly fat.

The observed link between belly fat and bad nutrients, such as cholesterol, was not affected by the gut microbiota. In contrast, we found that the gut microbiota plays an important role in the beneficial effect of good nutrients, such as fibre or vitamin E.

We show that specific gut bacteria play an important role in linking certain beneficial nutrients to less belly fat.

Published in Genome Biology , the study looked at data from 1, twins from the biobank TwinsUK. It found that people with a more diverse range of gut microbes had lower levels of visceral fat. Wait, but why look at data from twins? A missing part of the puzzle could be in the microbiome.

Projects like MetaSUB aim to look at the interaction between our environment and microbiome composition, but a large part of our microbiome is inherited — as this BioArtist explored in her work.

To add to the complexity, our genes can also impact the microbiome — indirectly contributing to obesity. The researchers describe several microbes and human genes that play a role in higher visceral fat.

Their exact mechanisms still have to be discovered, but understanding them could help develop new solutions for obesity — joining the first wave of microbiome-based therapies already fighting for approval.

Skip to content. Search for:. Suggested Topics:. Of note, a recent study showed that chronic hyperinsulinemia leads to premature adipocyte senescence and a pro-inflammatory secretory profile in vitro and in vivo In line with this, gut barrier dysfunction and increased gut permeability, which results in the impairment of biological homeostasis by the translocation of bacterial toxins inducing systemic inflammation, may be a major factor related to these conditions Thus, gut dysbiosis can affect the intestinal epithelial barrier by the modulation of the immune system, including TLR signaling, which regulates the integrity of tight junction complexes Remarkably, some modulators of intracellular tight junctions and gut permeability, such as zonulin, may also play a crucial role Accordingly, increased circulating levels of zonulin, an important marker of tight junction disassembly and increased gut permeability, have been correlated with gut dysbiosis and the development of metabolic disturbances 63 — Apart from gut dysbiosis, additional factors, such as diet, should be taken into consideration in the pathogenesis of gut permeability and pro-inflammatory response in obesity and T2D With regard to the influence of the gut microbiome on adipose tissue, Bäckhed et al.

reported for the first time that the gut microbiota was a key environmental factor in the predisposition towards adiposity, since it can regulate body fat storage and adipocyte metabolism Indeed, the causative role of gut microbiota in the development of obesity is supported by mice models, which showed that an obese phenotype could be transferred through fecal microbiota transplantation 67 , Notably, a number of studies have revealed that some gut microbial patterns have a strong influence on adipose tissue inflammation, which constitutes one of the essential features in adipocyte dysfunction and may also lead to beta cell impairment, as previously described.

In animal models, specific gut microbiota profiles have been demonstrated to drive Western-type diet-induced adipose tissue inflammation via myeloid differentiation primary response 88 Myd88 and TLR signaling Besides, increased intestinal permeability due to dysbiosis triggers the translocation of bacterial endotoxins that may have deleterious effects on adipose tissue.

In line with this, intestinal permeability has been associated with increased visceral lipid deposition in healthy women Also, elevated serum levels of lipopolysaccharide LPS from the Gram-negative bacterial membrane promote the inflammatory reaction in adipose tissue in obesity, including the pro-inflammatory activation of macrophages and adipocyte death by pyroptosis Gut dysbiosis leads to the release of zonulin, which modulates immune response and increases gut permeability in distinct metabolic disorders, including obesity 64 , Of note, low serum levels of zonulin have been associated with high alpha diversity in pregnant women with obesity Importantly, disruptions in the microbiome-immune-metabolic axis in early life, including gut barrier alterations and secondary immune-mediated inflammatory chronic activation related to childhood obesity, could impact adult overweight and obesity On the other hand, a growing body of evidence shows that the gut microbiome has a major role in the pathophysiology of T2D Thus, bacterial genera such as Ruminococcus , Fusobacterium , and Blautia have been positively associated with this condition, whereas Bifidobacterium , Bacteroides, Faecalibacterium, Akkermansia , and Roseburia are inversely related to T2D Moreover, increased gut permeability derived from gut dysbiosis may be related to the pathogenesis of T2D, as shown in preclinical studies In this regard, higher zonulin levels have been reported in patients with a recent diagnosis of T2D, and may play a role in the pathophysiology of this disease, although further research is needed Interestingly, preclinical studies show that the loss of some beneficial bacteria, such as Akkermansia muciniphila , causes impaired intestinal integrity and systemic inflammation, leading to insulin resistance, while the increased abundance of this bacterium restores normal insulin response Also, circulating levels of zonulin have been shown to be closely related to insulin resistance in clinical studies 64 , On the other side, clinical studies have revealed that calorie restriction may ameliorate insulin sensitivity through positive changes in the gut microbiota Further research in humans has also corroborated that gut microbiota composition is closely linked to insulin resistance 80 , In addition, animal models have shown that gut microbiota is required for early beta cell development and proliferation 82 , and gut microbiota signals e.

In animal models showing that an obese phenotype can be transferred by fecal microbiota transplantation, mild glucose intolerance was an early manifestation in the host, a fact that suggests that the gut microbiome may affect both adipose tissue and beta cell function Importantly, beta cell hyperactivity and subsequent hyperinsulinemia, which has a strong influence on adipose tissue dysfunction, can be transmitted early to recipient mice of obese microbiota despite only a minor increase in weight gain and adiposity Also, hyperglycemia may increase gut permeability, which could aggravate metabolic inflammation and lead to the development of adipose tissue dysfunction and obesity Remarkably, gut microbiota-related metabolites have direct effects on adipocyte and beta cell function Figure 2.

The gut microbiota secretes several molecules that reach key cells through specific receptors. By the fermentation of non-digestible dietary fibers, gut microbes produce SCFAs, including propionate, acetate, and butyrate, which exert direct actions through cell-surface G-protein-coupled receptors GPCRs Additional bacterial products, such as amino acids, triglyceride metabolites, and BAs can also target these receptors On the one hand, acetate was proven to inhibit glucose-stimulated insulin secretion via FFA2 and FFA3 in mouse and human beta cells Conversely, another study showed that acetate enhances glucose-stimulated insulin secretion through the activation of the parasympathetic nervous system, although these effects appear to be related to hyperphagia, ectopic lipid deposition, and insulin resistance Further studies have confirmed that acetate stimulates insulin secretion 88 , Butyrate may prevent pro-inflammatory cytokine-beta cell dysfunction and induce insulin secretion 90 , 91 , whereas propionate improved beta cell function and insulin release in humans 92 , although contrary results have also been described Besides, transmembrane bile acid receptor Takeda G-protein coupled receptor 5 TGR5 can enhance insulin secretion and improve glucose homeostasis 94 , FFA2 and FFA3 are also expressed by adipocytes and are mainly associated with the regulation of adipokine release and adipose tissue metabolism 96 , SCFAs may also induce the browning of adipose tissue Interestingly, butyrate can modulate adipocyte expansion and favor adipogenesis and adiponectin production through the upregulation of peroxisome proliferator-activated receptor gamma PPAR-γ 99 and suppresses adipocyte inflammation via the inhibition of the NOD-like receptor family pyrin domain containing 3 NLRP3 pathway Similarly, propionate ameliorates adipose tissue inflammation , whilst acetate could lead to adipose tissue dysfunction by TNF - α-induced MCP-1 production Figure 2 The potential role of gut microbiota-derived metabolites in beta cell and adipocyte function.

The gut microbiome secretes several signaling molecules with direct effects on beta cell and adipocyte function. Short-chain fatty acids SCFAs , including acetate, butyrate, and propionate, exert different effects on beta cells via binding short-chain fatty acid receptor-2 FFA2 and FFA3.

Thus, SCFAs inhibit apoptosis, improve beta cell function, and enhance insulin secretion. However, it has been reported that some SCFAs i.

Bile acids may stimulate insulin secretion and improve glucose homeostasis through Takeda G-protein coupled receptor 5 TGR5. SCFAs also have a role in adipocyte function via FFA2 and FFA3. Therefore, acetate, butyrate, and propionate regulate adipocyte metabolism and adipokine balance.

These effects may result in reciprocal influences between beta cells and the adipocyte. In previous sections, we have discussed the role of lipotoxicity, adipose tissue inflammation, and altered adipokine expression in the development of beta cell dysfunction and insulin resistance.

Since pathological shifts in gut microbiota composition and related metabolites may lead to adipose tissue dysfunction via the aforementioned mechanisms, derived consequences are expected in beta cell survival and function.

Thus, Faecalibacterium prausnitzii decreases adipocyte inflammation and increases adiponectin expression in visceral adipose tissue, which is related to insulin-sensitizing effects Similarly, A. muciniphila reverses adipose tissue inflammation and restores insulin sensitivity in T2D In addition, Akkermansia has been shown to be an important predictor of serum levels of FFAs, which are involved in lipotoxicity and beta cell impairment, presenting an inverse relationship with them and the pro-inflammatory cytokine IL-6 Notably, in a study evaluating the role of angiopoietin-like 4 ANGPTL4 in metabolic dysfunction, the loss of the expression of this adipokine uncoupled visceral fat accumulation from glucose intolerance via the gut microbiota Gut microbiome-derived metabolites are also important intermediates of the adipose tissue-beta cell crosstalk.

Tryptophan-derived compounds produced by the gut microbiota regulate miRNA expression in white adipose tissue, involved in glucose tolerance and insulin sensitivity Thus, a decrease in tryptophan-derived metabolites is associated with the overexpression of miRNA, which favors the development of adipose tissue inflammation, impaired glucose tolerance, and insulin resistance It is also known that butyrate stimulates adipocyte differentiation and adiponectin expression, favoring insulin sensitivity , whereas propionate enhances leptin expression and reduces resistin expression, which are closely involved in beta cell function Thus, elevated circulating levels of LPS in individuals with T2D activate TLR-2 expression and trigger immune response and inflammation in adipose tissue Metabolic endotoxemia induced by LPS triggers insulin resistance and the subsequent expression of inflammatory markers in adipose tissue to a similar extent as a high-fat diet In light of the above, gut dysbiosis and impaired metabolite secretion appear to drive an altered adipokine balance and induce adipose tissue inflammation, a fact that ultimately results in insulin resistance and beta cell dysfunction, which can also aggravate adipocyte inflammation via the gut microbiota, perpetuating the vicious cycle.

However, further mechanisms, such as the direct bacterial presence in adipose tissue, constituting a specific-tissue microbiota, have been postulated in this intricate relationship. Accordingly, in animal models, the presence of bacteria in adipose tissue was previously reported In mice, a high-fat diet induced the translocation of Gram-negative bacteria through intestinal mucosa to circulation and mesenteric adipose tissue via pathogen-associated molecular patterns PAMPs recognition, Myd88 signaling, and leptin regulation, resulting in low-grade inflammation, linked to the early stages of T2D Conversely, the identification of bacterial DNA in human adipose tissue has been a challenging task Recently, the presence of specific microbial signatures in three different adipose tissues omental, mesenteric, and subcutaneous adipose tissue has been identified in subjects with morbid obesity, varying between individuals with and without T2D, with more evident signatures in mesenteric adipose tissue, including a decrease of health-promoting bacteria, such as Faecalibacterium and increased abundance of pathogens e.

In addition, Massier et al. also detected bacterial DNA in omental, mesenteric, and subcutaneous adipose tissue from 75 participants with obesity with or without T2D Once more, mesenteric adipose tissue presented the highest bacterial quantity, which was associated with adipose tissue inflammation, and adipose tissue microbiota composition was different between subjects with and without diabetes However, devoted clinical studies are needed to confirm these results.

The gut microbiome may be targeted to modulate the metabolic dialogue between adipose tissue and pancreatic beta cells. Hence, prebiotic approaches [i. Oligofructose supplementation in high-fat diet-fed mice increased gut Bifidobacterium spp.

and prevented the elevation of adipose tissue inflammatory markers, which was linked to the improvement of glucose tolerance and the restoration of glucose-induced insulin secretion Moreover, an oligofructose-enriched diet decreased Firmicutes and increased Bacteroidetes abundance, reducing adipose lipid peroxidation and ameliorating leptin sensitivity and glucose tolerance On the other hand, the direct administration of health-promoting live microorganisms probiotics could confer several benefits.

Lactic acid bacteria strains were demonstrated to modulate the adipokine profile in in vitro models muciniphila and F. prausnitzii , may constitute an attractive approach , , Postbiotics, defined as bioactive substances produced by microorganisms with positive effects on the host , can also modulate adipocyte and beta cell function.

The previously discussed SCFAs are relevant postbiotics in this regard 85 , , The combination of inulin and SCFAs reduced adipocyte size and prevented diet-induced obesity and insulin resistance in animal models Interestingly, the administration of the natural metabolite 4-cresol reduced adiposity and enhanced insulin secretion and beta cell proliferation in mouse islets Fecal microbiota transplantation from lean donors to patients with obesity and metabolic syndrome transiently improved insulin sensitivity , and animal models have revealed that this therapy may reverse beta cell dysfunction However, further research is needed to confirm these results.

Obesity and T2D are increasing in prevalence, resulting in major health and socioeconomic consequences. The relationships between these two disorders are well established; however, some of the underlying mechanisms involved in their pathophysiology and bidirectional links are not fully understood.

Pancreatic beta cells and adipose tissue are closely interconnected through the presence of a number of bioactive hormones and intricate signaling pathways. Also, the gut microbiome may play a key role in the mediation of the complex dialogue between the adipocyte and beta cell, with derived potential therapeutic strategies in this field.

However, important issues are yet to be elucidated. Cells do not live in isolation, and multiple interactions are expected to occur beyond the dialogue among the gut microbiome, adipose tissue, and pancreatic beta cells. Therefore, additional players, such as the skeletal muscle and the liver, may be included in this metabolic crosstalk.

Future perspectives in this area should also focus on the development of therapeutic approaches e. Finally, dedicated clinical studies are warranted to fully unravel the role of the gut microbiome and related metabolites in the crosstalk between pancreatic beta cells and adipose tissue.

Conceptualization, JM-M and FT. Investigation, JM-M, MD-F, and JF-G. Original draft preparation, JM-M and MD-F. Writing- review and editing, JM-M, JF-G, and FT. Supervision, FT. All authors contributed to the article and approved the submitted version.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. GBD Obesity Collaborators, Afshin A, Forouzanfar MH, Reitsma MB, Sur P, Estep K, et al.

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There are as many, if not more, bacteria in and on a human body as there are human cells. Over the past few decades, we have been slowly untangling how these bacteria influence our health , fend against infections , and even change our brains. A study in showed that, after accounting for all other factors, obese people had a slightly less diverse set of gut bacteria than lean people.

First they looked at data from more than 3, twins to find out whether visceral fat—the body fat stored around the waist—is a good indicator of obesity. Using twins helps researchers determine how much genetic versus environmental factors affect a condition.

They found that it was. They also obtained stool samples from 1, of the twins, which they analyzed to understand what types of bacteria lived in their guts. That analysis, published in Genome Biology , gave them two results. First, a certain proportion of gut bacteria seem to be inherited.

Second, people with less bacterial diversity in their gut had a higher proportion of visceral fat—confirming, in other words, the finding that obesity is correlated with having less diverse gut bacteria.

But a study in mice hints that it might be the case. In that study, researchers bred mice in bacteria-free environments. Then one mouse got gut bacteria implanted from those of an obese woman, while the other mouse got bacteria from her lean twin sister.

The observed link between belly fat and bad nutrients, such as cholesterol, was not affected by the gut microbiota.

In contrast, we found that the gut microbiota plays an important role in the beneficial effect of good nutrients, such as fibre or vitamin E. We show that specific gut bacteria play an important role in linking certain beneficial nutrients to less belly fat.

Diet alone did not have a strong impact on the observed links between gut microbes and belly fat, as specific gut bacteria were linked to belly fat accumulation regardless of diet. This confirms what was previously seen in mice, that gut microbiota alone could affect fat accumulation.

Our findings also provide further evidence that the human gut microbiota plays an important role in the individualised response to food. A limitation of our study was that we analysed measurements taken at a single point in time. This means that we cannot establish causal links.

Another drawback is that most people misreport what they eat. Researchers are working on improving the way that diet is reported, which should lead to more accurate work in the future.

Our results mean that in the future, you may need to have your gut microbiota checked so that your doctor or dietitian can give you personalised dietary advice. Although bacteria may be partially to blame for the rise in rates of obesity, until we know more it is best to stick to a healthy, varied diet rich in fibre, fruit and vegetables, which in turn may result in a healthier gut microbiota.

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