Metabolic effects of secretin

Sekar, Revathi; Chow, Billy K. C.

doi:10.1016/j.ygcen.2012.11.017

Cited by 17 publications

(11 citation statements)

References 118 publications

(115 reference statements)

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“…Among hormones that stimulate lipolysis, such as catecholamines, insulin, glucagon, growth hormone, and thyroid hormone (5, 6), the lipolytic effect of Sct remains elusive (23–28). Being a recently recognized anorectic hormone (20) with elevated plasma concentrations during fasting, as shown in our study and other studies (38–40), along with increased SctR expression in the epididymal adipose tissue during fasting (Fig. 1B), we therefore hypothesized the potential function of Sct in lipid metabolism.…”

Section: Discussionsupporting

confidence: 79%

“…This reinforces the relevance and importance of the need for more research on Sct and lipid metabolism. Our group and others have recently highlighted the importance of reevaluating the metabolic effects of Sct (20, 56). In this report, we have provided evidence to conclude that Sct has an acute lipolytic effect in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

“…More recently, the role of Sct as a neuroactive peptide has been substantiated (11, 13–15) and it has been found to regulate, at multiple levels, in osmoregulation (16–19). Although Sct has recently been shown to be an anorectic peptide (20, 21), its metabolic role in regulating lipolysis remains a controversial issue. There is evidence supporting (22–25) and some negating (26–28) the lipolytic effects of Sct.…”

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confidence: 99%

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Lipolytic actions of secretin in mouse adipocytes

Sekar

Chow

2014

Journal of Lipid Research

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Secretin (Sct), a classical gut hormone, is now known to play pleiotropic functions in the body including osmoregulation, digestion, and feeding control. As Sct has long been implicated to regulate metabolism, in this report, we have investigated a potential lipolytic action of Sct. In our preliminary studies, both Sct levels in circulation and Sct receptor (SctR) transcripts in adipose tissue were upregulated during fasting, suggesting a potential physiological relevance of Sct in regulating lipolysis. Using SctR knockout and Sct knockout mice as controls, we show that Sct is able to stimulate lipolysis in vitro in isolated adipocytes dose- and time-dependently, as well as acute lipolysis in vivo. H-89, a protein kinase A (PKA) inhibitor, was found to attenuate lipolytic effects of 1 μM Sct in vitro, while a significant increase in PKA activity upon Sct injection was observed in the adipose tissue in vivo. Sct was also found to stimulate phosphorylation at 660ser of hormone sensitive lipase (HSL) and to bring about the translocation of HSL from cytosol to the lipid droplet. In summary, our data demonstrate for the first time the in vivo and in vitro lipolytic effects of Sct, and that this function is mediated by PKA and HSL.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Lipolytic actions of secretin in mouse adipocytes

Sekar

Chow

2014

Journal of Lipid Research

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“…Secretin, a 27-amino acid peptide, was the first hormone discovered, in 1902 by Bayliss and Starling a finding that initiated the field of endocrinology. 18, 19 The major site of production of secretin is the endocrine S cells located in the proximal small intestinal mucosa. 20 Secretin is secreted by the gut in response to fatty acid or acidic pH containing food.…”

Section: Introductionmentioning

confidence: 99%

Validation of SCT Methylation as a Hallmark Biomarker for Lung Cancers

Zhang

Ma²,

Sathe³

et al. 2016

Journal of Thoracic Oncology

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Background The human secretin (SCT) gene encodes secretin, a hormone with limited tissue distribution. Analysis of The Cancer Genome Atlas (TCGA) 450K methylation array data indicated that the SCT promoter region is differentially hypermethylated in lung cancer. Our purpose was to validate SCT methylation as a potential cancer biomarker for lung cancer. Methods We analyzed TCGA data, and developed and applied SCT-specific bisulfite DNA sequencing and quantitative methylation specific PCR (qMSP) assays. Results The analyses of TCGA 450K data of 801 samples showed that SCT hypermethylation has an area under curve (AUC) value >0.98 to distinguish lung adenocarcinomas or squamous cell carcinomas from non-malignant lung. We confirmed the highly discriminative SCT methylation by bisulfite sequencing of lung cancer cell lines and normal blood cells. By applying qMSP, we found that SCT hypermethylation was frequently detected in all major subtypes of malignant NSCLC (AUC=0.92, n=108) and SCLC cancers (AUC=0.93, n=40) but less frequently present in lung carcinoids (AUC=0.54, n=20). SCT hypermethylation appeared in lung carcinoma in situ samples during multistage pathogenesis and increased in invasive samples. Further analyses of TCGA 450K data showed that SCT hypermethylation is highly discriminative in most types of other malignant tumors but less frequently present in low-grade malignant tumors. The only normal tissue with high methylation was the placenta. Conclusions Our findings demonstrated that SCT methylation is a highly discriminative biomarker for lung and other malignant tumors, and less frequently present in low-grade malignant tumors including lung carcinoids, and appears at the carcinoma in situ stage.

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“…The gut hormone secretin is released from S‐cells in the epithelium of the duodenum into the circulation during a meal and controls pancreatic and gastric functions required for digestion and resorption of food. Meanwhile, several metabolic effects of secretin have been demonstrated, including stimulation of bile secretion, lipolysis in adipocytes, and satiation . We recently demonstrated that the meal‐associated surge of serum secretin directly activates brown fat thermogenesis, independent of beta‐adrenergic receptor signaling in the tissue .…”

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confidence: 99%

Secretin Links Brown Fat to Food Intake: New Perspectives for Targeting Energy Balance in Humans

Klingenspor

2019

Obesity

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In 1902, Neumann referred to the concept of Luxuskonsumption in his habilitation thesis, essentially stating that we can dissipate excess nutritional energy as heat to keep slim: "On the other hand, we also know very well that someone who otherwise 'lives well' consumes a sufficient amount of food and in the process enters into a luxury consumption in the organism" (1)*. Sixty years later, the thermogenic function of brown fat was first recognized, leading to significant research efforts to address the role of the sympathetic nervous system for cold-and diet-induced thermogenesis in brown fat. Recruitment and activation of brown fat thermogenesis was envisioned as a feasible strategy to promote negative energy balance and lose weight. In retrospect, research targeting brown fat for obesity therapy has been characterized by phases of skepticism and enthusiasm, with the latter currently prevailing (2). To date, however, it remains unclear whether sufficient brown fat capacity for energy expenditure can be recruited in people with obesity to reduce body weight effectively (3). In the positive case, this would require that increased brown fat thermogenesis is not fully compensated by increasing food intake (4). Ten years ago, landmark publications reported on the presence of cold-inducible brown fat in human adults (5). Cold-inducible activation of human brown fat is impaired with age and in people with obesity and type 2 diabetes, whereas cold acclimation initiates remission in association with improved metabolic homeostasis. In principle, given the current estimate of more than 300 g, total brown fat mass in humans could significantly promote negative energy balance if permanently active (6). Our lifestyle in thermoneutral environments, however, normally precludes cold-induced brown fat activation.Other than cold-induced thermogenesis, resting metabolic rate is also increased in association with a meal, known as the thermal effect of food. This effect is partially due to the obligatory costs of digestion and resorption, which depend on the macronutrient composition and caloric density of meals. However, as a facultative component, brown fat is also activated during meal ingestion. A recent study demonstrated that a single mixed meal activates human brown fat to the same degree as cold exposure (7). While obligatory costs of food digestion and resorption are inevitable, the reason for meal-associated thermogenesis in brown fat remains unclear. In this context, previous research pointing at a role of brown fat in the control of food intake may provide an answer. The hypothetical framework of thermoregulatory feeding implies that episodic events of brown fat activation are responsible for meal initiation and termination (8). The drop of core body temperature during a nonfeeding interval eventually triggers a burst of sympathetic nerve activity, stimulating brown fat thermogenesis. Concomitant glucose uptake into brown fat from the circulation results in hypoglycemia, which is sensed in the brain and initiates feeding....

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Metabolic effects of secretin

Cited by 17 publications

References 118 publications

Lipolytic actions of secretin in mouse adipocytes

Lipolytic actions of secretin in mouse adipocytes

Validation of SCT Methylation as a Hallmark Biomarker for Lung Cancers

Secretin Links Brown Fat to Food Intake: New Perspectives for Targeting Energy Balance in Humans

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