RT journal article
T1 Genetic deficiency of apolipoprotein D in the mouse is associated with nonfasting hypertriglyceridemia and hyperinsulinemia
A1 Perdomo, Germán
A1 Jiménez Palomares, Margarita
A1 Cozar Castellano, Irene
A1 Ganfornina, Maria Dolores
A1 Sanchez, Diego
A1 Perdomo, Germán
A2 BiomedicinaBiotecnología y Salud Pública
AB Apolipoprotein D (ApoD) is an atypical apolipoprotein with an incompletely understoodfunction in the regulation of triglyceride and glucose metabolism. We have demonstratedthat elevated ApoD production in mice results in improved postprandial triglycerideclearance. This work studies the role of ApoD deficiency in the regulation of triglycerideand glucose metabolism and its dependence on aging. We used ApoD knockout (ApoD-KO)mice of 3 and 21 months of age. Body weight and food intake were measured. Hepatichistology, triglyceride content, lipoprotein lipase levels, and plasma metabolites werestudied. Phenotypic characterization of glucose metabolism was performed using glucosetolerance test. β-Cell mass, islet volume, and islet number were analyzed byhistomorphometry. Apolipoprotein D deficiency results in nonfasting hypertriglyceridemiain young (P = .01) and aged mice (P = .002). In young ApoD-KO mice, hypertriglyceridemiawasassociated with 30% to 50% increased food intake in nonfasting and fasting conditions,respectively, without changes in body weight. In addition, lipoprotein lipase levels werereduced by 35% in adipose tissue (P = .006). In aged ApoD-KO mice, hypertriglyceridemia wasnot associated with changes in food intake or body weight, whereas hepatic triglyceridelevels were reduced by 35% (P = .02). Furthermore, nonfasting plasma insulin levels wereelevated by 2-fold in young (P = .016) and aged (P = .004) ApoD-KO mice, without changes inblood glucose levels, glucose tolerance, β-cell mass, or islet number. These findingsunderscore the importance of ApoD in the regulation of plasma insulin levels andtriglyceride metabolism, suggesting that ApoD plays an important role in the pathogenesisof dyslipidemia.
PB Elsevier
SN 0026-0495
YR 2011
FD 2011
LK http://hdl.handle.net/10498/33449
UL http://hdl.handle.net/10498/33449
LA eng
DS Repositorio Institucional de la Universidad de Cádiz
RD 10-nov-2026