About this Research Topic
The enteroendocrine cell (EEC) system is the biggest endocrine organ of the human body.
Specifically, it is composed of a heterogeneous family of electrically-excitable nutrient-responsive hormone-producing cells dispersed along the mucosa of the gastrointestinal (GI) tract. Traditionally the EEC system has been divided into at least twelve independent cell types, based on their hormonal content. Nonetheless, recent topographical molecular dissection renders this distinction outdated. The current paradigm sees cells expressing hormonal gradients with a specific spatio-temporal, crypt-to-villus and rostro-caudal distribution.
Collectively the EECs are responsible for the production of more than 30 peptidic hormones released in the systemic circulation to regulate the intermediary metabolism in response to the GI tract luminal content. Furthermore, some specific sub-families of EEC engage via direct synapses with neurons of the enteric nervous system (ENS) or the central nervous system (CSN) to modulate the physiology of different organs such as β-cells in the pancreas, or the hypothalamus in the brain.
Type 2 Diabetes (T2D) in obese people defines a condition known as diabesity, and it currently represents the biggest epidemic the human population is facing. Diabesity is primarily caused by physical inactivity and hyper caloric diets rich in saturated lipids and fast absorbing simple carbohydrates. Affected patients display among other abnormalities, functional modifications in the enteroendocrine cell system. Indeed, only in the last decade the complex relationship between diet and the EEC system in healthy or diabetic individuals has started to be unraveled.
The chronic exposure to a complex diet-dependent cocktail of EEC-modulating agents appears to be one of the key causative agents of obesity and T2D. Topographic reorganization of the GI tract, as seen in surgical procedures such as Roux-en-Y gastric by-pass (RYGB) or Sleeve gastrectomy (SLG) aimed to reduce the absorptive surface of the obese and diabetic patients’ guts, represents today the most successful and straightforward cure for diabetes. The post-surgical GI hormonal fingerprint have been reported in small number of patients, nonetheless lacking statistical power to draw a clear hormonal-fingerprint. This special issue aims to better define the physio-pathological role of the enteroendocrine cell system, exploring pharmacological solutions aimed to correct pathologies like type 2 diabetes and related cardiovascular co-morbidities such as atherosclerosis.
Specifically, it is composed of a heterogeneous family of electrically-excitable nutrient-responsive hormone-producing cells dispersed along the mucosa of the gastrointestinal (GI) tract. Traditionally the EEC system has been divided into at least twelve independent cell types, based on their hormonal content. Nonetheless, recent topographical molecular dissection renders this distinction outdated. The current paradigm sees cells expressing hormonal gradients with a specific spatio-temporal, crypt-to-villus and rostro-caudal distribution.
Collectively the EECs are responsible for the production of more than 30 peptidic hormones released in the systemic circulation to regulate the intermediary metabolism in response to the GI tract luminal content. Furthermore, some specific sub-families of EEC engage via direct synapses with neurons of the enteric nervous system (ENS) or the central nervous system (CSN) to modulate the physiology of different organs such as β-cells in the pancreas, or the hypothalamus in the brain.
Type 2 Diabetes (T2D) in obese people defines a condition known as diabesity, and it currently represents the biggest epidemic the human population is facing. Diabesity is primarily caused by physical inactivity and hyper caloric diets rich in saturated lipids and fast absorbing simple carbohydrates. Affected patients display among other abnormalities, functional modifications in the enteroendocrine cell system. Indeed, only in the last decade the complex relationship between diet and the EEC system in healthy or diabetic individuals has started to be unraveled.
The chronic exposure to a complex diet-dependent cocktail of EEC-modulating agents appears to be one of the key causative agents of obesity and T2D. Topographic reorganization of the GI tract, as seen in surgical procedures such as Roux-en-Y gastric by-pass (RYGB) or Sleeve gastrectomy (SLG) aimed to reduce the absorptive surface of the obese and diabetic patients’ guts, represents today the most successful and straightforward cure for diabetes. The post-surgical GI hormonal fingerprint have been reported in small number of patients, nonetheless lacking statistical power to draw a clear hormonal-fingerprint. This special issue aims to better define the physio-pathological role of the enteroendocrine cell system, exploring pharmacological solutions aimed to correct pathologies like type 2 diabetes and related cardiovascular co-morbidities such as atherosclerosis.
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