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Plasma Immunoreactive Somatostatin is Elevated in Diabetic Ketoacidosis and Correlates with Plasma Non‐esterified Fatty Acid Concentration
Author(s) -
Binimelis J.,
Webb S. M.,
Serrano J.,
Codina M.,
Corcoy R.,
Perez A.,
Peinado M. A.,
Puig M.,
Torre W.,
Serrat J.,
Gomez J. A.,
Casamitjana R.,
Leiva A.
Publication year - 1987
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.1987.tb00866.x
Subject(s) - nefa , medicine , endocrinology , diabetic ketoacidosis , ketoacidosis , ketone bodies , diabetes mellitus , insulin , basal (medicine) , somatostatin , ketogenesis , metabolism , type 1 diabetes
In experimental diabetes and after the administration of β‐hydroxybutyrate and non‐esterified fatty acids (NEFA), an increase in circulating immunoreactive somatostatin (IRS) has been described. Both ketones and NEFA are raised in diabetic ketoacidosis. Therefore, we decided to investigate 10 patients in diabetic ketoacidosis by measuring, on admission and throughout the initial 24 hours of therapy, circulating levels of IRS, β‐hydroxybutyrate, acetoacetate, triglycerides, blood glucose, pH and NEFA. Fluids and insulin were administered IV following a previously established protocol. Nine patients showed abnormally high levels of circulating IRS. When compared with a group of controlled insulin‐dependent diabetic patients, basal IRS was high (111 ± 15 vs 28 ± 3 pmol/l), and remained elevated for at least 24 h despite clear improvement of metabolic status. On admission we also found elevated levels of NEFA (1.04 ± 0.2 mmol/l), triglycerides (4.7 ± 1.1 mmol/l), β‐hydroxybutyrate (22.1 ± 4mmol/l), and acetoacetate (4.8 ± 1.1 mmol/l). A significant correlation was found initially between IRS and NEFA ( p <0.01). We conclude that circulating IRS is high in most cases of diabetic ketoacidosis. The mechanism behind this hypersomatostatinaemia could be related to the abnormalities of lipid metabolism which occur in diabetic ketoacidosis.