Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 1.3.8.1 extracted from

  • Pepin, E.; Guay, C.; Delghingaro-Augusto, V.; Joly, E.; Madiraju, S.R.; Prentki, M.
    Short-chain 3-hydroxyacyl-CoA dehydrogenase is a negative regulator of insulin secretion in response to fuel and non-fuel stimuli in INS832/13 beta-cells (2010), J. Diabetes, 2, 157-167.
    View publication on PubMed

Cloned(Commentary)

Cloned (Comment) Organism
gene HADHSC, real-time quantitative PCR expression analysis in in INS832/13 beta-cells Homo sapiens

Protein Variants

Protein Variants Comment Organism
additional information knockdown of HADHSC expression by RNA interference in INS832/13 beta-cells using short hairpin RNA and short interference RNA Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
INS-1 823/13 cell
-
Homo sapiens
-

Synonyms

Synonyms Comment Organism
HADHSC
-
Homo sapiens
short-chain 3-hydroxyacyl-CoA dehydrogenase
-
Homo sapiens

General Information

General Information Comment Organism
malfunction patients with mutated beta-oxidation enzyme short-chain 3-hydroxyacyl-CoA dehydrogenase show hyperinsulinemia associated with non-ketotic hypoglycemia, analysis of the mechanism underlying HADHSC-mediated regulation of insulin secretion, overview. Enhanced glucose-stimulated insulin secretion induced by HADHSC knockdown is independent of changes in cytosolic Ca2+ and also occurs in the presence of fatty acids. The pan transaminase inhibitor amino-oxyacetate reverses HADHSC knockdown-mediated increases in glucose-stimulated insulin secretion. Oxidation of palmitate and octanoate is not reduced in HADHSC knockdown cells. L-3-Hydroxybutyryl-carnitine and L-3-hydroxyglutarate, which accumulate in blood and urine, respectively, of HADHSC-deficient patients, do not change insulin secretion. Transamination reaction(s) and the formation of short-chain acylcarnitines and CoAs may be implicated in the mechanism whereby HADHSC deficiency results in enhanced insulin secretion and hyperinsulinemia Homo sapiens