Metabolic Endotoxemia Initiates Obesity and Insulin Resistance
Open accessAbstract
Diabetes and obesity are two metabolic diseases characterized by insulin resistance and a low-grade inflammation. Seeking an inflammatory factor causative of the onset of insulin resistance, obesity, and diabetes, we have identified bacterial lipopolysaccharide (LPS) as a triggering factor. We found that normal endotoxemia increased or decreased during the fed or fasted state, respectively, on a nutritional basis and that a 4-week high-fat diet chronically increased plasma LPS concentration two to three times, a threshold that we have defined as metabolic endotoxemia. Importantly, a high-fat diet increased the proportion of an LPS-containing microbiota in the gut. When metabolic endotoxemia was induced for 4 weeks in mice through continuous subcutaneous infusion of LPS, fasted glycemia and insulinemia and whole-body, liver, and adipose tissue weight gain were increased to a similar extent as in high-fat–fed mice. In addition, adipose tissue F4/80-positive cells and markers of inflammation, and liver triglyceride content, were increased. Furthermore, liver, but not whole-body, insulin resistance was detected in LPS-infused mice. CD14 mutant mice resisted most of the LPS and high-fat diet–induced features of metabolic diseases. This new finding demonstrates that metabolic endotoxemia dysregulates the inflammatory tone and triggers body weight gain and diabetes. We conclude that the LPS/CD14 system sets the tone of insulin sensitivity and the onset of diabetes and obesity. Lowering plasma LPS concentration could be a potent strategy for the control of metabolic diseases.
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The low-grade chronic inflammation state in metabolic syndrome has been explained by metabolic endotoxemia resulting from gut dysbiosis.
“Primary, the low-grade chronic inflammation state in MetS has been explained by the metabolic endotoxemia that was a result of gut dysbiosis [6,7].”
From Effects of Regular Kefir Consumption on Gut Microbiota in Patients with Metabolic Syndrome: A Parallel-Group, Randomized, Controlled Study (2019) · cites this paper as [7]
MAFLD patients exhibit increased permeability of intestinal barriers, which can lead to translocation of commensal metabolites, bacterial components and bacteria themselves, resulting in systemic inflammation.
“MAFLD patients exhibit increased permeability of intestinal barriers, which can lead to translocation of commensal metabolites, bacterial components and bacteria themselves, resulting in systemic inflammation (Cani et al., 2007).”
From <i>Akkermansia muciniphila</i> alleviates <scp>high‐fat‐diet</scp> ‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids (2023) · cites this paper as Cani et al., 2007
Leakage of microbial products such as lipopolysaccharide causes metabolic endotoxemia.
“Leakage of microbial products, such as the endotoxin lipopolysaccharide (LPS), causes metabolic endotoxemia.101”
From Influence of the Gut Microbiome, Diet, and Environment on Risk of Colorectal Cancer (2020) · cites this paper as [101]
A high-fat diet increases intestinal permeability in mice, with a two-to-three-fold increase in systemic lipopolysaccharide levels.
“High-fat diet increases intestinal permeability in mice with a two-to-three-fold increase in systemic LPS levels62.”
From The gut microbiome and liver cancer: mechanisms and clinical translation (2017) · cites this paper as [62]
Mice chronically exposed to low levels of LPS for four weeks gained weight and became insulin-resistant.
“Interestingly, mice chronically exposed to low levels of LPS for four weeks gained weight and became insulin-resistant (Cani et al., 2007).”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Cani et al., 2007
Once in circulation, LPS elicits a potent inflammatory response via Toll-like 4 receptor signaling, which has been implicated in the development of cardiovascular and metabolic disease.
“Once in circulation, LPS elicits a potent inflammatory response via Toll-like 4 receptor signaling, which has been implicated in the development of cardiovascular and metabolic disease (34).”
From The gut microbiota at the intersection of diet and human health (2018) · cites this paper as [34]
Circulating LPS from gastrointestinal bacteria may contribute to insulin resistance.
“LPS also signals through TLR4 (in concert with the CD14 receptor), and a recent study found that circulating LPS derived from gastrointestinal bacteria could play a role in insulin resistance.”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [118]
Mice lacking Cd14 are protected from high-fat-diet-induced insulin resistance.
“These workers found increased circulating levels of gut-derived LPS in HFD-fed mice and demonstrated that mice with KO of Cd14, which is a receptor for LPS, were protected from HFDinduced insulin resistance (118).”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [118]
High-fat-diet-fed mice have higher circulating levels of gut-derived LPS.
“These workers found increased circulating levels of gut-derived LPS in HFD-fed mice and demonstrated that mice with KO of Cd14, which is a receptor for LPS, were protected from HFDinduced insulin resistance (118).”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [118]
Dysbiosis is associated with increased intestinal permeability, known as leaky gut syndrome.
“Dysbiosis is associated with increased intestinal permeability, which is known as the “leaky gut syndrome” (Figure 3) [112,113,114,115,116].”
From Bone diseases in patients with chronic liver disease (2019) · cites this paper as [115]
Metabolic endotoxemia, defined as a 2- to 3-fold elevation of circulating endotoxin/lipopolysaccharide level, has been proposed as an initiating factor of obesity-related cardiometabolic dysfunction.
“Metabolic endotoxemia, defined as a 2-to 3-fold elevation of the circulating endotoxin/lipopolysaccharide level, has been proposed as an initiating factor of obesity-related cardiometabolic dysfunction.”
High-fat fed mice exhibited an increase in body weight and inflammatory markers as well as a decrease in glucose tolerance.
“As expected, high-fat fed mice exhibited an increase in body weight and inflammatory markers as well as a decrease in glucose tolerance.”
From Gut Microbiota Contribute to Age-Related Changes in Skeletal Muscle Size, Composition, and Function: Biological Basis for a Gut-Muscle Axis (2018) · cites this paper as [18]
Circulating levels of LPS were 2- to-3-fold elevated in high-fat fed mice when compared with control fed animals.
“circulating levels of lipopolysaccharide (LPS), a component of the outer membrane of gram negative bacteria, were 2- to-3-fold elevated in high-fat fed mice when compared with control fed animals.”
From Gut Microbiota Contribute to Age-Related Changes in Skeletal Muscle Size, Composition, and Function: Biological Basis for a Gut-Muscle Axis (2018) · cites this paper as [18]
In wild-type and CD-14 mutant mice subjected to LPS infusion, pro-inflammatory cytokine induction and impairments in glucose tolerance were observed exclusively in the wild-type animals.
“pro-inflammatory cytokine induction and impairments in glucose tolerance were observed exclusively in the wild-type animals.”
From Gut Microbiota Contribute to Age-Related Changes in Skeletal Muscle Size, Composition, and Function: Biological Basis for a Gut-Muscle Axis (2018) · cites this paper as [18]
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- Authors
- Cani, P. D., Amar, J., Iglesias, M. A., Poggi, M., Knauf, C., Bastelica, D., Neyrinck, A. M., Fava, F., Tuohy, K. M., Chabo, C., Waget, A., Delmée, E., Cousin, B., Sulpice, T., Chamontin, B., Ferrières, J., Tanti, J.-F., Gibson, G. R., Casteilla, L., Delzenne, N. M., Alessi, M. C., & Burcelin, R.
- Affiliations
- UCLouvain (BE)
- Inserm (FR)
- Institute of Molecular Medicine, I2MR Toulouse, France
- University of Reading (GB)
- Unité Pharmacokinetics, Metabolism, Nutrition, and Toxicology-73/69, Université catholique de Louvain, Brussels, Belgium
- Unité Mixte de Recherche 5241, Centre National de la Recherche Scientifique, Université Paul Sabatier, Toulouse, France
- Physiogenex (France) (FR)
- Institut National de la Santé et de la Recherche Médicale (INSERM) 558, Toulouse, France
- INSERM U 568, Nice, France
- Centre National de la Recherche Scientifique (FR)
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2007-07-01
- Volume
- 56
- Issue
- 7
- Pages
- 1761-1772
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2131536322
- Cited by
- 6,638
- References
- 47
- Citations by year
- 2026: 491 · 2025: 407 · 2024: 456 · 2023: 449 · 2022: 536 · 2021: 537 · 2020: 575 · 2019: 456 · 2018: 396 · 2017: 391 · 2016: 380 · 2015: 351 · 2014: 282 · 2013: 269 · 2012: 197
- FWCI
- 71.14
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- other-oa
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- eCite Digital Repository (University of Tasmania) (submittedVersion)
- Digital Access to Libraries (submittedVersion, other-oa)
- Figshare (submittedVersion, cc-by)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- metabolic endotoxemia, lipopolysaccharide, CD14, insulin resistance, obesity, type 2 diabetes, gut microbiota, high-fat diet, fasting, adipose tissue inflammation, hepatic triglycerides, low-grade inflammation
- MeSH terms
- Animals, Dietary Fats, Insulin Resistance, Lipopolysaccharides, Male, Obesity, Lipopolysaccharide Receptors, Endotoxemia, Mice
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