Overnutrition-induced metabolic disorders are the major driving force of metabolic syndrome, which refers to a cluster of risk factors including hyperglycemia, dyslipidemia, abdominal obesity, and hypertension. Metabolic syndrome has been regarded as an inflammatory disorder, which is characterized by chronic low-grade inflammation. Overproduction of the proinflammatory cytokines TNF-a and IL-1ß increased the risk for the occurrence and development of diseases like obesity, type 2 diabetes, fatty liver, and cardiovascular disease. Of note, metabolites from food, dietary ingredients, and natural products are essential regulators of the immune response. For example, the ketogenic diet exhibits anti-inflammatory properties and contributes to alleviating hepatic steatosis. Increased dietary intake of saturated fat triggers inflammatory processes in the intestine, adipose, and liver. Moreover, suppression of inflammatory signaling pathways, such as NF-?B/NLRP3 pathway has been proposed for the prevention and treatment of the high fat diet-induced metabolic syndrome. Thus, future studies to understand the mechanism of the immune response, and identify key inflammatory drivers and anti-inflammatory approaches are critically important to the development of treatments for overnutrition-induced metabolic disorders.
The goal of this Research Topic is to provide a forum to advance research on the contribution of immune response (intestine, liver, adipose tissues, pancreas, etc.) to the occurrence and development of overnutrition-induced metabolic syndrome as well as to explore anti-inflammatory strategies in the attempt to achieve a beneficial impact on metabolic syndrome.
The submission of Original Research and Review articles is welcome here including, but not limited to, the following subtopics:
1) Effects of metabolites from food, dietary ingredients, and natural products on immune response during the development of the metabolic syndrome;
2) Mechanisms of immune responses of nutrient metabolism organs, such as intestine, liver, adipose tissues, and pancreas, in overnutrition-induced metabolic syndrome;
3) Identification of inflammatory signaling pathways and mediators during the development of the metabolic syndrome;
4) Potential strategy to treat low-grade chronic inflammation of metabolic syndrome.
Overnutrition-induced metabolic disorders are the major driving force of metabolic syndrome, which refers to a cluster of risk factors including hyperglycemia, dyslipidemia, abdominal obesity, and hypertension. Metabolic syndrome has been regarded as an inflammatory disorder, which is characterized by chronic low-grade inflammation. Overproduction of the proinflammatory cytokines TNF-a and IL-1ß increased the risk for the occurrence and development of diseases like obesity, type 2 diabetes, fatty liver, and cardiovascular disease. Of note, metabolites from food, dietary ingredients, and natural products are essential regulators of the immune response. For example, the ketogenic diet exhibits anti-inflammatory properties and contributes to alleviating hepatic steatosis. Increased dietary intake of saturated fat triggers inflammatory processes in the intestine, adipose, and liver. Moreover, suppression of inflammatory signaling pathways, such as NF-?B/NLRP3 pathway has been proposed for the prevention and treatment of the high fat diet-induced metabolic syndrome. Thus, future studies to understand the mechanism of the immune response, and identify key inflammatory drivers and anti-inflammatory approaches are critically important to the development of treatments for overnutrition-induced metabolic disorders.
The goal of this Research Topic is to provide a forum to advance research on the contribution of immune response (intestine, liver, adipose tissues, pancreas, etc.) to the occurrence and development of overnutrition-induced metabolic syndrome as well as to explore anti-inflammatory strategies in the attempt to achieve a beneficial impact on metabolic syndrome.
The submission of Original Research and Review articles is welcome here including, but not limited to, the following subtopics:
1) Effects of metabolites from food, dietary ingredients, and natural products on immune response during the development of the metabolic syndrome;
2) Mechanisms of immune responses of nutrient metabolism organs, such as intestine, liver, adipose tissues, and pancreas, in overnutrition-induced metabolic syndrome;
3) Identification of inflammatory signaling pathways and mediators during the development of the metabolic syndrome;
4) Potential strategy to treat low-grade chronic inflammation of metabolic syndrome.
