Inquiry Basket
Loading ......
Secretin was the first hormone ever discovered. Secretin is primarily produced by enteroendocrine S cells located in the duodenum and upper jejunum. Traditionally, Secretin has been recognized as a gastrointestinal hormone involved in digestive regulation. When acidic chyme enters the small intestine from the stomach, S cells release Secretin into circulation, stimulating the exocrine pancreas to secrete bicarbonate-rich fluid that neutralizes gastric acid and protects the intestinal mucosa.
For decades, Secretin was viewed mainly as a digestive hormone. Its biological profile is now understood to extend far beyond gastrointestinal physiology. Secretin participates in multiple metabolic processes, including:
These functions place Secretin among the gut-derived hormones involved in systemic metabolic regulation and metabolic syndrome research.
Fig. 1 Physiological effects of secretin
Metabolic syndrome (MetS) is a multifactorial metabolic disorder characterized by a cluster of interconnected cardiometabolic abnormalities. Current treatment strategies are often fragmented, requiring separate therapies for glucose control, lipid regulation, and blood pressure management. Increasing attention has therefore shifted toward upstream metabolic regulators capable of influencing multiple pathways simultaneously.
The gastrointestinal tract functions as a major endocrine organ that coordinates nutrient sensing and systemic metabolism through gut-derived peptide hormones. Hormones such as GLP-1, GIP, and Secretin connect nutrient intake with:
Within this endocrine network, Secretin has emerged as a signaling molecule with potential relevance to obesity-associated disorders.
The biological actions of Secretin are mediated through the Secretin receptor (SCTR), a member of the Class B G protein-coupled receptor (GPCR) family. Although initially associated mainly with pancreatic and gastrointestinal tissues, SCTR expression has also been identified in:
This broad tissue distribution supports the role of Secretin in systemic metabolic regulation.
Binding of Secretin to SCTR activates Gs protein signaling, stimulating adenylate cyclase and increasing intracellular cyclic AMP (cAMP) levels.
The downstream activation of protein kinase A (PKA) regulates several metabolic processes, including:
In adipose tissue, Secretin signaling has been associated with enhanced mitochondrial activity and increased expression of uncoupling protein 1 (UCP1), a central mediator of adaptive thermogenesis.
Fig. 2 Secretin-SCTR signaling pathway
One of the most important areas of Secretin research involves its role in brown adipose tissue (BAT) activation and thermogenesis.
Brown adipose tissue is a metabolically active fat depot specialized for heat production. Unlike white adipose tissue (WAT), which primarily stores triglycerides, BAT contains abundant mitochondria and expresses high levels of UCP1.
UCP1 enables mitochondria to dissipate chemical energy as heat rather than storing it as ATP, thereby increasing total energy expenditure.
Circulating Secretin levels increase after meal intake and directly stimulate BAT activity through SCTR signaling. Secretin-mediated BAT activation is associated with:
These metabolic effects link Secretin to meal-induced thermogenesis and postprandial energy dissipation.
In addition to activating classical BAT, Secretin may also promote the browning or beiging of white adipose tissue.
WAT browning refers to the conversion of white adipocytes into beige adipocytes with thermogenic properties similar to BAT. This process is associated with:
Because impaired energy expenditure and visceral fat accumulation are hallmarks of metabolic syndrome, Secretin-induced thermogenesis and adipose tissue remodeling may contribute to obesity intervention strategies.
Body weight regulation depends not only on peripheral metabolism but also on central nervous system control of feeding behavior.
Secretin functions as part of the gut–brain axis involved in satiety signaling and appetite regulation.
Secretin regulates feeding behavior through coordinated communication between the intestine, brown adipose tissue, and hypothalamus. The proposed pathway involves:
This integrated signaling network is commonly referred to as the Gut-Brain-BAT axis.
Fig. 3 Secretin-Activated Brown Fat Mediates Prandial Thermogenesis to Induce Satiation
Secretin receptors are expressed in hypothalamic regions associated with energy homeostasis and appetite control. Secretin signaling may influence neuronal pathways involved in:
By integrating peripheral thermogenic signals with central appetite regulation, Secretin may help prevent chronic caloric excess and obesity progression.
Although Secretin has historically been linked to exocrine pancreatic function, it also participates in endocrine and metabolic regulation.
Secretin may influence glucose homeostasis through interactions with pancreatic endocrine pathways and other gut hormones. Potential metabolic effects include:
Secretin is less potent than GLP-1 in stimulating insulin secretion, but it may function cooperatively with other gut-derived hormones to support balanced metabolic responses following nutrient intake.
The liver is a major metabolic organ involved in glucose production, glycogen storage, and lipid metabolism. Secretin signaling may influence:
These pathways are highly relevant to non-alcoholic fatty liver disease (NAFLD), a common complication of obesity and metabolic syndrome. By improving systemic energy balance and lipid handling, Secretin-related signaling may help reduce metabolic stress associated with hepatic steatosis and insulin resistance.
The clinical success of gut hormone-based therapies has accelerated interest in Secretin as a potential metabolic therapeutic target.
Secretin signaling influences multiple metabolic processes simultaneously, including:
This multifunctional profile makes Secretin an attractive candidate for obesity and metabolic syndrome intervention.
One major limitation of endogenous Secretin is its extremely short circulating half-life due to rapid enzymatic degradation and renal clearance.
To overcome these challenges, researchers are developing:
Long-acting Secretin analogs
Selective SCTR agonists
Modified peptide therapeutics
These approaches aim to improve pharmacokinetic stability and metabolic efficacy.
Combination therapies targeting multiple gut hormone pathways are becoming an important direction in metabolic disease research.
Secretin-based co-agonism strategies may complement GLP-1-mediated effects by combining:
Such approaches may help overcome adaptive metabolic slowing that often limits long-term weight loss success.
As interest in gut hormone therapeutics continues to expand, Secretin and SCTR signaling are becoming increasingly important areas in obesity and metabolic syndrome research.
Secretin has evolved from a classical digestive hormone into an important regulator of systemic metabolism. Through its effects on brown adipose tissue activation, thermogenesis, appetite regulation, and glucose and lipid metabolism, Secretin influences several key mechanisms underlying metabolic syndrome. Continued research into Secretin biology and SCTR signaling may support the development of new therapeutic strategies for obesity, insulin resistance, and related metabolic disorders.
DPAB-CS24757 Secretin Pab
IHC of paraffin-embedded human stomach tissue using Secretin antibody at dilution of 1:50
DPABH-01117 SCTR (a.a. 188-280) Pab
IHC of paraffin-embedded mouse thyroid tissue using Secretin receptor antibody at dilution of 1:200
DPABH-28328 SCT (a.a. 19-121) Pab
Recombinant Protein lysates were subjected to SDS PAGE followed by WB with SCT Pab at 1 µg/ml.
DPABH-25384 SCTR Pab
Human liver cancer tissue were subjected to SDS PAGE followed by WB with SCTR Pab at dilution of 1:600
References
| Target | Cat. No. | Product Name | Host | Species Reactivity | Application | |
| SCT | DCABH-13378 | Anti-SCT Mab | Rabbit | Human | WB, ELISA | Inquiry |
| DPAB3264RH | Anti-SCT (a.a.14-27) Pab | Rabbit | Human | ELISA | Inquiry | |
| DPABH-28328 | Anti-SCT (a.a. 19-121) Pab | Rabbit | Mouse | WB | Inquiry | |
| CPBT-65790RH | Anti-SCT Pab | Rabbit | Human, Pig | ELISA, IHC-P | Inquiry | |
| DPAB-CS24757 | Anti-SCT Pab | Rabbit | Human, Pig | IHC | Inquiry | |
| SCTR | DCABH-13379 | Anti-SCTR Mab | Rabbit | Human | WB, ELISA | Inquiry |
| CABT-12121MH | Anti-SCTR Mab, clone 4I2 | Mouse | Human | WB, ELISA | Inquiry | |
| DPABH-06708 | Anti-SCTR (full length) Pab | Mouse | Human | WB | Inquiry | |
| DPABH-01117 | Anti-SCTR (a.a. 188-280) Pab | Rabbit | Mouse, Human, Rat, Dog, Cow, Rabbit, Sheep | IHC-P, IHC-F, IF | Inquiry | |
| DPABH-25384 | Anti-SCTR (a.a. 120-169) Pab | Rabbit | Human | WB | Inquiry |
Loading ......
