Effects of cholecystokinin, secretin, and pancreatic polypeptide on secretion of gastric inhibitory polypeptide, insulin, and glucagon

Williams, Robert H.; Champagne, James

doi:10.1016/0024-3205(79)90500-9

Cited by 35 publications

(5 citation statements)

References 22 publications

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“…GLP-1 and CCK are intestinal incretins; that is, proteins that stimulate pancreatic insulin secretion 52–54. GPR120 activation can induce GLP-1 and CCK secretion, which may further regulate pancreatic islet function and β-cell proliferation and survival.…”

Section: Role Of Gpr120 In Regulating Cell and Tissue Functionsmentioning

confidence: 99%

Potential roles of GPR120 and its agonists in the management of diabetes

Zhang¹,

Leung²

2014

DDDT

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Free fatty acids (FFAs) serve not only as nutrients that provide energy but also as extracellular signaling molecules that manipulate intracellular physiological events through FFA receptors (FFARs) such as FFAR4. FFAR4 is also known as G-protein coupled receptor 120 (GPR120). The main role of GPR120 is to elicit FFA regulation on metabolism homeostasis. GPR120 agonism correlates with prevention of the occurrence and development of metabolic disorders such as obesity and diabetes. GPR120 activation directly or indirectly inhibits inflammation, modulates hormone secretion from the gastrointestinal tract and pancreas, and regulates lipid and/or glucose metabolism in adipose, liver, and muscle tissues, which may help prevent obesity and diabetes. This review summarizes recent advances in physiological roles of GPR120 in preventing insulin resistance and protecting pancreatic islet function, and examines how resident GPR120 in the pancreas may be involved in modulating pancreatic islet function.

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Section: Role Of Gpr120 In Regulating Cell and Tissue Functionsmentioning

confidence: 99%

Potential roles of GPR120 and its agonists in the management of diabetes

Zhang¹,

Leung²

2014

DDDT

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“…In healthy subjects, plasma glucagon is increased by hypoglycemia (56), mixed meals (57), arginine infusion (41,56,57), or a-adrenergic stimulation (58); is decreased by glucose administration (59,60); and is unchanged (41,(61)(62)(63)(64) by secretin. Less predictable patterns, however, are found in tumor-bearing patients.…”

Section: Summer 1981mentioning

confidence: 99%

The Glucagonoma Syndrome: Clinical Features, Diagnosis, and Treatment

1981

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Historical BackgroundIslet cell tumors of the pancreas have been described for over 50 yr. Although carcinoma arising from islet tissue had been noted since the turn of the century (1), not until 1927 was the first case of a hormonally active pancreatic neoplasm, an insulinoma, recorded (2). For many years thereafter, pancreatic endocrine tumors were characterized as either insulin-producing or "nonfunctional," the latter being derived from cells apparently devoid of clinically significant hormonal activity. With time, however, other islet cell secretory products were discovered and their tumors identified with various clinical syndromes. Whereas the hypoglycemia of insulinomas and hyperacidity of gastrinomas figured prominently in the initial recognition of these neoplasms, the clinical signs of glucagon-producing tumors were less readily apparent and not as easily attributable to specific hormone excess.Becker and co-workers (3) are credited with the first description of a glucagonoma. Their case, reported in 1947 but diagnosable only in retrospect, typifies what is now regarded as a classic clinical presentation of the syndrome. The patient, a 45-yr-old woman, sought attention because of a skin rash that, over a period of 8 months, progressed to involve almost her entire body. Weight loss, weakness, and amenorrhea were additional complaints. The rash was symmetrically distributed and characterized by confluent, pruritic areas of macular, erythematous, and vesicular erruptions showing evidence of exfoliation and superficial necrosis. Stomatitis and onchonolysis were also found. Laboratory examination revealed a normochromic anemia, mild fasting hyperglycemia, and hypoproteinemia. Deep venous thrombosis developed while the patient was in hospital, and she succumbed to cardiorespiratory failure. At autopsy, an islet cell neoplasm was discovered "replacing the body

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“…Phe-NH 2 ) accounts for 60% of the CCK family expressed in the human body and exhibits stronger activity than CCK33; in rats, it induces gallbladder contraction and amylase secretion in the pancreatic acini. [6][7][8][9] Binding site of CCK with its specific receptors is known to exist around the C-terminal region, which involves two methionine (Met) residues, 28 Met and 31 Met. We previously reported that the hydroxyl radical generated in vitro (Fenton's reaction) or hydrogen peroxide (H 2 O 2 ) can oxidize 28 Met and 31 Met of CCK8 to produce a CCK8 sulfoxide or sulfone [ Fig.…”

Section: Introductionmentioning

confidence: 99%