A Glucagonoma Syndrome

Mallinson, C. N.; Bloom, Stephen R.; Warin, A P; Salmon, P. R.; Cox, Brian D.

doi:10.1016/s0140-6736(74)91343-9

Cited by 465 publications

(177 citation statements)

References 23 publications

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“…Our study shows that whole-body protein breakdown is increased in glucagonoma patients, and this alteration could have a pivotal role in the loss of lean body mass commonly observed in this syndrome [1]. Previous reports on the effects of acute hyperglucagonaemia in healthy humans did not find any significant stimulation of postabsorptive whole-body proteolysis [3,4].…”

Section: Discussionsupporting

confidence: 55%

“…This observation emphasizes the increment of protein breakdown, which would be quantitatively even greater if normalized per body nitrogen content. Whereas muscle wasting is one of the hallmarks of glucagonoma [1], in previous reports glucagon had minor shortterm effects on in vivo skeletal muscle protein metabolism [8]. Again, prolonged hyperglucagonaemia and hypoaminoacidaemia might specifically enhance muscle proteolysis.…”

Section: Discussionmentioning

confidence: 97%

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mentioning

confidence: 99%

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Protein metabolism in glucagonoma

et al. 1999

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Patients with glucagon-producing pancreatic tumours exhibit profound metabolic disturbances, leading to the typical glucagonoma syndrome [1]. In particular, weight loss, muscle mass reduction and hypoaminoacidaemia suggest a sustained protein catabolism probably due, at least in part, to glucagon excess. Indeed, acute hyperglucagonaemia in healthy humans reduced plasma amino acid concentration [2] and enhanced essential amino acid catabolism [3,4], although no effects on whole-body proteolysis were detected in the presence of basal insulin concentrations [3,4]. Rather surprisingly, when leucine and protein kinetics were studied in a patient with glucagonoma, only a slight increase of leucine oxidation was reported, and protein breakdown was normal [5]. This patient had been treated, however, with i. v. octreotide and amino acids, which might have influenced protein turnover during the study [6]. Therefore, the mechanisms leading to protein wasting in glucagonoma are still not completely understood. To investigate this issue, postabsorptive leucine, phenylalanine and tyrosine kinetics were studied in two glucagonoma patients prior to treatment, and compared with normal control subjects values. Diabetologia (1999) Plasma leucine, phenylalanine and tyrosine rates of appearance in patients with glucagonoma were similar to values in the control subjects, except leucine rate of appearence in the female patient with glucagonoma ( + &30 %, d > 2 SD). In contrast, the intracellular leucine rate of appearence, reflecting protein degradation, was considerably increased in both patients ( + 60±80 %, d > 2 SD). Phenylalanine hydroxylation was moderately higher only in the male patient with glucagonoma ( + &30 %, d > 2 SD). Leucine, phenylalanine and tyrosine clearances ( + 100±300 %), as well as phenylalanine hydroxylative clearance ( + 75±100 %) were also increased in the patients. In conclusion, whole-body protein breakdown is enhanced in patients with glucagonoma compared with healthy control subjects. Phenylalanine hydroxylative clearance is also higher. Reduced plasma amino acid concentrations are probably due, at least in part, to their increased clearance. These alterations could contribute to the determination of the catabolic state of the glucagonoma syndrome. [Diabetologia (1999) 42: 326±329]

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 97%

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Protein metabolism in glucagonoma

et al. 1999

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“…However, Barnes et al (1975) were unable to demonstrate that glucagon played any major role in the control of blood sugar levels in insulin-dependent diabetics, although high levels of glucagon may be responsible for inducing ketosis (Alberti et al 1975). Certainly in glucagonomas, excessively high levels of glucagon lead only to mild diabetes without obvious ketoacidosis (Mallinson et al 1974).…”

Section: Table2 Hormones Involvedin Glucoslasismentioning

confidence: 99%

The Nature of Diabetes

Bloom

1978

J R Soc Med

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“…Glucagonomas have been described in association with the syndrome of a characteristic necrolytic migratory erythematous rash, mild diabetes,anaemia, glossitis, stomatitis, and weight loss (Mallinson et al, 1974). Relief of symptoms has followed removal of an isolated pancreatic adenoma (Lightman and Bloom, 1974).…”

Section: Tumours Secreting Enterohormonesmentioning

confidence: 99%

Tests of Exocrine Pancreatic Function

Gowenlock

1977

Ann Clin Biochem

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A Glucagonoma Syndrome

Cited by 465 publications

References 23 publications

Protein metabolism in glucagonoma

Protein metabolism in glucagonoma

The Nature of Diabetes

Tests of Exocrine Pancreatic Function

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