title: Serum levels of leptin and changes during the course of recovery from diabetic ketoacidosis.
abstract: Secretion of leptin, the obese gene product, is stimulated by insulin and glucocorticoids and reduced by fasting. In subjects with diabetic ketoacidosis (DKA), severe insulinopenia and prolonged fasting might cause a decrease in serum leptin levels, and subsequent insulin therapy would reverse the decrease. Otherwise, some other confounding factors, neither insulin nor fasting, might affect serum leptin levels in patients with DKA. The present study was undertaken to address these issues. Eleven patients with type 1 diabetes mellitus (seven males and four females, aged 44+/-6 years, mean +/- SEM), admitted to Jichi Medical School Hospital presenting DKA, were studied during the therapeutic period. Thirty-five sex-, age- and body mass index-matched healthy subjects served as controls. Serum leptin levels at the hospitalization were significantly greater than those of the matched control subjects (5.5+/-1.0 vs. 3.2+/-0.3 microg/l, P < 0.01). After the start of therapy with a small dose of short-acting insulin and a large volume of fluid infusion, serum leptin concentrations further increased to 10.6+/-3.6 microg/l at 24 h, and thereafter the concentrations gradually decreased and normalized at the discharge (3.3+/-0.7 microg/l, day 24+/-4). The peak levels at 24 h were significantly higher than the levels at the discharge (P < 0.05), and also +77+/-34% higher than those at the hospitalization (P < 0.005). Serum cortisol levels (1830+/-200 nmol/l) were markedly elevated at hospitalization. These results indicate that serum leptin levels are increased even under insulinopenia and fasting in the patients with DKA. Such a finding may be associated with marked hyperglycemia or enhanced secretion of glucocorticoid hormone, although the exact mechanisms remain to be elucidated. We speculate that leptin may serve as a stress peptide in DKA, but further analysis is necessary to explore a physiological role of leptin in DKA.
authors.affiliation: Department of Medicine, Jichi Medical School, Tochigi, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: S
authors.initials: S
authors.lastname: Nagasaka
authors.forename: S
authors.initials: S
authors.lastname: Ishikawa
authors.forename: K
authors.initials: K
authors.lastname: Fujibayashi
authors.forename: A
authors.initials: A
authors.lastname: Kawakami
authors.forename: K
authors.initials: K
authors.lastname: Rokkaku
authors.forename: H
authors.initials: H
authors.lastname: Hayashi
authors.forename: T
authors.initials: T
authors.lastname: Saito
authors.forename: I
authors.initials: I
authors.lastname: Kusaka
authors.forename: M
authors.initials: M
authors.lastname: Higashiyama
authors.forename: T
authors.initials: T
authors.lastname: Saito
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology; D016883:Diabetic Ketoacidosis / Q000097:blood* / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use*; D007657:Ketone Bodies / Q000097:blood; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D007657:Ketone Bodies; D020738:Leptin