Triglyceride Metabolism in Acute Starvation: The Role of Secretin and Glucagon

Stout, Robert W.; Hoggart, Richard; Buchanan, K. D.

doi:10.1111/j.1365-2362.1976.tb00509.x

Cited by 43 publications

(19 citation statements)

References 37 publications

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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%

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%

Lipolytic actions of secretin in mouse adipocytes

Sekar

Chow

2014

Journal of Lipid Research

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“…Further, the response of an organism to a metabolic stress, such as starvation, is largely dependent on its capacity to derive energy from stored reserves like triglyceride (lipid) [9, 10] and glycogen (glucose) [11, 12]. Genetic perturbations that impinge on lipid metabolism have been implicated as one of the causes of metabolic deregulation, and often associated with obesity and type II diabetes [13-16].…”

Section: Introductionmentioning

confidence: 99%

dSir2 deficiency in the fatbody, but not muscles, affects systemic insulin signaling, fat mobilization and starvation survival in flies

Banerjee

Ayyub

Sengupta

et al. 2012

Aging

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Sir2 is an evolutionarily conserved NAD+ dependent protein. Although, SIRT1 has been implicated to be a key regulator of fat and glucose metabolism in mammals, the role of Sir2 in regulating organismal physiology, in invertebrates, is unclear. Drosophila has been used to study evolutionarily conserved nutrient sensing mechanisms, however, the molecular and metabolic pathways downstream to Sir2 (dSir2) are poorly understood. Here, we have knocked down endogenous dSir2 in a tissue specific manner using gene-switch gal4 drivers. Knockdown of dSir2 in the adult fatbody leads to deregulated fat metabolism involving altered expression of key metabolic genes. Our results highlight the role of dSir2 in mobilizing fat reserves and demonstrate that its functions in the adult fatbody are crucial for starvation survival. Further, dSir2 knockdown in the fatbody affects dilp5 (insulin-like-peptide) expression, and mediates systemic effects of insulin signaling. This report delineates the functions of dSir2 in the fatbody and muscles with systemic consequences on fat metabolism and insulin signaling. In conclusion, these findings highlight the central role that fatbody dSir2 plays in linking metabolism to organismal physiology and its importance for survival.

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“…Cortisol and growth hormone were measured by an in-house direct radioimmunoassay. Insulin (Hales & Randle, 1963), glucagon (Stout et al, 1976) and pancreatic polypeptide (O'Hare et al, 1983) were measured by radioimmunoassay. All samples for each subject were analysed in one run with intra-assay coefficients of variations of: glucagon 11.1%, adrenaline 6%, growth hormone 6.8%, insulin 9% and cortisol 6%.…”

Section: Glucose Clampmentioning

confidence: 99%

Beta‐adrenoceptor blockade and hypoglycaemia. A randomised, double‐ blind, placebo controlled comparison of metoprolol CR, atenolol and propranolol LA in normal subjects.

Kerr¹,

Macdonald²,

Heller³

et al. 1990

Brit J Clinical Pharma

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1. The effect of 1 week of treatment with propranolol LA (160 mg), atenolol (100 mg) and metoprolol CR (100 mg) on awareness of and the physiological responses to moderate hypoglycaemia were compared with placebo using a randomised, cross‐over design in 12 healthy volunteers. 2. All three beta‐adrenoceptor antagonists reduced resting heart rate, systolic blood pressure and heart rate responses to submaximal exercise compared with placebo. 3. Under hyperinsulinaemic (60 mu m‐2 min‐1) clamp conditions, at a blood glucose of 2.5 mmol l‐1, atenolol prevented the rise in systolic and atenolol and metoprolol CR prevented the fall in diastolic blood pressure usually associated with hypoglycaemia. At this level of hypoglycaemia, the expected increase in heart rate was inhibited by atenolol but not metoprolol CR. Pre‐ treatment with propranolol LA resulted in a significant pressor response and a bradycardia during hypoglycaemia. In addition the normal increase in finger tremor was abolished by propranolol LA. 4. During hypoglycaemia all three beta‐adrenoceptor blockers augmented sweating compared with placebo but hypoglycaemic symptoms, awareness and slowing of reaction time were the same with drugs and placebo. 5. The rise in plasma adrenaline and other counter‐regulatory hormones during hypoglycaemia was enhanced by beta‐adrenoceptor blockade. 6. We conclude that beta‐adrenoceptor antagonists modify the physiological and hormonal responses to, but do not adversely affect awareness of, moderate hypoglycaemia in healthy volunteers.

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Triglyceride Metabolism in Acute Starvation: The Role of Secretin and Glucagon

Cited by 43 publications

References 37 publications

Lipolytic actions of secretin in mouse adipocytes

Lipolytic actions of secretin in mouse adipocytes

dSir2 deficiency in the fatbody, but not muscles, affects systemic insulin signaling, fat mobilization and starvation survival in flies

Beta‐adrenoceptor blockade and hypoglycaemia. A randomised, double‐ blind, placebo controlled comparison of metoprolol CR, atenolol and propranolol LA in normal subjects.

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