- Part 1 Principles of international endocrine practice
- Part 2 Pituitary and hypothalamic diseases
- Part 3 The thyroid
- Part 4 Parathyroid, calcium, and bone metabolism
- Part 5 The adrenal gland and endocrine hypertension
- Part 6 Neuroendocrine tumours and genetic disorders
- 6.1 Neuroendocrine tumours of the gastrointestinal tract: an appraisal of the past and perspectives for the future
- 6.2 Neuroendocrine tumour markers
- 6.3 Neuroendocrine (carcinoid) tumours and the carcinoid syndrome
- 6.4 Gastrinoma
- 6.5 Insulinoma and hypoglycaemia
- 6.6 Glucagonoma
- 6.7 VIPomas
- 6.8 Somatostatinoma
- 6.9 Imaging neuroendocrine tumours of the gastrointestinal tract
- 6.10 Systemic mastocytosis
- 6.11 Multiple endocrine neoplasia type 1
- 6.12 Multiple endocrine neoplasia type 2
- 6.13 von Hippel–Lindau disease and succinate dehydrogenase subunit (SDHB, SDHC, and SDHD) genes
- 6.14 Neurofibromatosis
- 6.15 Carney’s complex
- 6.16 Molecular and clinical characteristics of the McCune–Albright syndrome
- 6.17 Cowden’s syndrome
- Part 7 Growth and development during childhood
- Part 8 Female endocrinology and pregnancy
- Part 9 Male hypogonadism and infertility
- Part 10 Endocrinology of ageing and systemic disease
- Part 11 Endocrinology of cancer
- Part 12 Obesity, lipids, and metabolic disorders
- Part 13 Diabetes mellitus
(p. 920) Glucagonoma
- Chapter:
- (p. 920) Glucagonoma
- Author(s):
G.M.K. Nijher
and S.R. Bloom
- DOI:
- 10.1093/med/9780199235292.003.0648
Glucagonomas are neuroendocrine tumours arising from the α cells of the islets of Langerhans, which result in excessive secretion of glucagon and peptides derived from preproglucagon. Post-translational modification of proglucagon is tissue specific and results in various glucagon peptides (1). It is the ratio of insulin to glucagon that controls the balance of gluconeogenesis and glycogenolysis in the liver. Glucagon stimulates hepatic gluconeogenesis and inhibits both glycolysis and glycogen synthesis. It increases production of free fatty acids from triglyceride breakdown by activating hormone-sensitive lipase; these undergo fatty oxidation in the liver via acetyl CoA, forming ketone bodies. The increase in free fatty acids from lipolysis inhibits hepatic lipogenesis. Glucagon also increases muscle proteolysis, resulting in an increase in amino acid supply to the liver.
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- Part 1 Principles of international endocrine practice
- Part 2 Pituitary and hypothalamic diseases
- Part 3 The thyroid
- Part 4 Parathyroid, calcium, and bone metabolism
- Part 5 The adrenal gland and endocrine hypertension
- Part 6 Neuroendocrine tumours and genetic disorders
- 6.1 Neuroendocrine tumours of the gastrointestinal tract: an appraisal of the past and perspectives for the future
- 6.2 Neuroendocrine tumour markers
- 6.3 Neuroendocrine (carcinoid) tumours and the carcinoid syndrome
- 6.4 Gastrinoma
- 6.5 Insulinoma and hypoglycaemia
- 6.6 Glucagonoma
- 6.7 VIPomas
- 6.8 Somatostatinoma
- 6.9 Imaging neuroendocrine tumours of the gastrointestinal tract
- 6.10 Systemic mastocytosis
- 6.11 Multiple endocrine neoplasia type 1
- 6.12 Multiple endocrine neoplasia type 2
- 6.13 von Hippel–Lindau disease and succinate dehydrogenase subunit (SDHB, SDHC, and SDHD) genes
- 6.14 Neurofibromatosis
- 6.15 Carney’s complex
- 6.16 Molecular and clinical characteristics of the McCune–Albright syndrome
- 6.17 Cowden’s syndrome
- Part 7 Growth and development during childhood
- Part 8 Female endocrinology and pregnancy
- Part 9 Male hypogonadism and infertility
- Part 10 Endocrinology of ageing and systemic disease
- Part 11 Endocrinology of cancer
- Part 12 Obesity, lipids, and metabolic disorders
- Part 13 Diabetes mellitus