We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Are gut dysbiosis, barrier disruption, and endotoxemia related to adipose tissue dysfunction in metabolic disorders? Overview of the mechanisms involved
Summary
Researchers reviewed how an imbalanced gut microbiome (dysbiosis) and a leaky gut barrier allow bacterial components to enter the bloodstream and trigger the low-grade inflammation that drives obesity and metabolic diseases like type 2 diabetes. The review highlights the gut-brain-fat tissue axis as a key pathway and calls for more research into how gut bacteria regulate metabolism and inflammation in peripheral tissues like fat.
Recently, compelling evidence points to dysbiosis and disruption of the epithelial intestinal barrier as major players in the pathophysiology of metabolic disorders, such as obesity. Upon the intestinal barrier disruption, components from bacterial metabolism and bacteria itself can reach peripheral tissues through circulation. This has been associated with the low-grade inflammation that characterizes obesity and other metabolic diseases. While circulating bacterial DNA has been postulated as a common feature of obesity and even type 2 diabetes, almost no focus has been given to the existence and effects of bacteria in peripheral tissues, namely the adipose tissue. As a symbiont population, it is expected that gut microbiota modulate the immunometabolism of the host, thus influencing energy balance mechanisms and inflammation. Gut inflammatory signals cause direct deleterious inflammatory responses in adipose tissue and may also affect key gut neuroendocrine mechanisms governing nutrient sensing and energy balance, like incretins and ghrelin, which play a role in the gut-brain-adipose tissue axis. Thus, it is of major importance to disclose how gut microbiota and derived signals modulate neuroendocrine and inflammatory pathways, which contribute to the dysfunction of adipose tissue and to the metabolic sequelae of obesity and related disorders. This review summarizes the current knowledge regarding these topics and identifies new perspectives in this field of research, highlighting new pathways toward the reduction of the inflammatory burden of metabolic diseases.
Sign in to start a discussion.
More Papers Like This
Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease
This review examines how environmental toxicants, including micro and nanoplastics, target fat tissue and contribute to metabolic diseases like obesity, diabetes, and fatty liver disease. These pollutants disrupt mitochondria (the energy-producing parts of cells) and trigger a cycle of oxidative stress and inflammation that damages both fat tissue and the liver. The findings suggest that microplastic exposure could be one of several environmental factors contributing to the rising rates of metabolic disease worldwide.
Immune mechanism of gut microbiota and its metabolites in the occurrence and development of cardiovascular diseases
This review examines immune mechanisms linking gut microbiota and its metabolites to cardiovascular diseases, explaining how disruptions in the microbiota-immune balance contribute to conditions such as atherosclerosis, hypertension, and heart failure.
Are microplastics in food a risk factor for obesity: Current evidence, mechanistic pathways and emerging health risks associated with human exposure
This review examines the emerging evidence linking microplastic and nanoplastic exposure to metabolic dysfunction and potential obesity risk. Researchers found that these particles have been detected in multiple human tissues and may contribute to inflammation, hormonal disruption, gut microbiome changes, and altered fat cell development. While animal and laboratory studies support a plausible connection, the study notes that direct evidence in humans is still limited and further research is needed.
Emerging mechanisms of microplastic-induced skin diseases: a perspective from the gut–skin axis
This review explores how microplastics may cause skin damage through the gut-skin axis, a system connecting intestinal and skin health through immunological and neuroendocrine pathways. The study suggests that microplastics can disrupt gut microbial balance and intestinal barrier integrity, allowing harmful bacteria and metabolites to enter the bloodstream and contribute to skin inflammation, metabolic imbalance, and oxidative stress.
Biological exposure to microplastics and nanoplastics and plastic additives: impairment of glycolipid metabolism and adverse effects on metabolic diseases
This review examines how exposure to micro- and nanoplastics disrupts the body's ability to process sugars and fats, potentially contributing to diabetes, obesity, and atherosclerosis. The plastics cause inflammation and oxidative stress, damage gut bacteria, trigger insulin resistance, and increase fat buildup in the liver. For people who already have metabolic conditions, plastic exposure may make their disease worse.