RGD Reference Report - Serum leptin and insulin in paediatric end-stage liver disease and following successful orthotopic liver transplantation. - Rat Genome Database

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Serum leptin and insulin in paediatric end-stage liver disease and following successful orthotopic liver transplantation.

Authors: Roberts, G A  Holt, R I  Ghatei, M A  Baker, A J  Bloom, S R  Miell, J P 
Citation: Roberts GA, etal., Clin Endocrinol (Oxf). 1998 Apr;48(4):401-6. doi: 10.1046/j.1365-2265.1998.00448.x.
RGD ID: 25330350
Pubmed: PMID:9640405   (View Abstract at PubMed)
DOI: DOI:10.1046/j.1365-2265.1998.00448.x   (Journal Full-text)


OBJECTIVE: Leptin, the product of the ob gene, is a postulated feedback regulator of adiposity with appetite suppressant and catabolic effects. Catabolic states are associated with decreased body fat mass as a result of both nutritional and metabolic perturbation. Low serum leptin has been described previously in a number of catabolic states. It has been unclear whether the observed changes in leptin are a cause or consequence of changes in adiposity. Paediatric end-stage liver disease (ESLD) is characterized by decreased body fat mass and poor linear growth. Successful treatment by orthotopic liver transplantation (OLT) is accompanied by increase in fat mass. We investigated the hypothesis that serum leptin would be low in paediatric ESLD and that increase in body fat mass post-OLT would result in increased serum leptin.
DESIGN: Serum leptin and insulin were measured by radioimmunoassay in children with ESLD before and after successful OLT and in age-matched controls.
PATIENTS: Twenty-four children with ESLD attending the outpatient department of King's College Hospital, London and 10 age-matched controls.
MEASUREMENTS: Anthropometric measurements were performed according to standard techniques and standard deviation (SDS) derived from population standards. Serum leptin and insulin were measured by radioimmunoassay.
RESULTS: Serum leptin pre-OLT, leptin (4.06 micrograms/l, [3.45, 5.68] median, with 25th and 75th interquartile ranges) was significantly lower than controls (6.62 micrograms/l, [4.33, 8.05], P = 0.02). Following OLT, serum leptin fell to levels which were significantly lower than pre-OLT values (3.32 micrograms/l, [2.30, 3.99], P = 0.01). There was no significant difference between boys and girls either pre-OLT (boys; 3.64 micrograms/l, [2.45, 5.57], girls; 4.14 micrograms/l, [3.18, 5.65]) or post-OLT (boys; 3.32 micrograms/l, [2.93, 3.62], girls; 3.69 micrograms/l, [2.23, 4.63]. Neither the age at OLT nor the age at the time of blood sampling was correlated with serum leptin pre-OLT or post-OLT. Pre-OLT the children were significantly malnourished with low measures of body fat mass (mid-arm circumference (MAC) SDS -1.90 [-4.67, -1.07]; triceps skinfold thickness (TSF) SDS -1.53, [-2.23, -0.23]; body mass index (BMI) 16.2, [15.5, 16.9]). Three months post-OLT, there were significant improvements in MAC SDS (-0.77, [-1.08, -0.20], P = 0.02) and TSF SDS (-0.41, [-1.95, -0.38], P = 0.003), but no significant change in BMI (15.9 [15.3, 16.7], P = 0.41. Pre-OLT, log serum leptin did not correlate with BMI, MAC SDS or TSF SDS. In contrast, post-OLT, there was a positive correlation between log serum leptin and BMI (r = 0.59, P = 0.003), MAC SDS (r = 0.49, P = 0.01) and TSF SDS (r = 0.41, P = 0.05). BMI also correlated with log serum leptin in the control children (r = 0.64, P = 0.04).
CONCLUSIONS: Serum leptin is low in children with end-stage liver disease but does not show the expected correlation with measures of body fat mass. Surprisingly, following orthotopic liver transplantation serum leptin falls significantly despite significant increases in measures of body fat mass (triceps skinfold thickness standard deviation scores, mid-arm circumference standard deviation scores). Orthotopic liver transplantation restores the expected correlation of serum leptin with measures of body fat mass within the treatment group. The elevation of serum leptin above predicted levels in paediatric end-stage liver disease offers a mechanism for the anorexia and cachexia characteristic of this disease.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
End Stage Liver Disease  IEP 25330350; 25330350; 25330350protein:decreased expression:serum (human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Lep  (leptin)

Genes (Mus musculus)
Lep  (leptin)

Genes (Homo sapiens)
LEP  (leptin)


Additional Information