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ADCK2 deficiency reduces weight gain and increases body temperature of mice in high fat diet

AuthorsHernández-Camacho, Juan Diego; Cascajo Almenara, M. V. ; López-Lluch, Guillermo ; Navas, Plácido
Issue Date2017
CitationJoint Congress (2017)
AbstractPrimary coenzyme Q (CoQ) deficiency causes a heterogenic group of mitochondrial diseases with high variability in severity and tissues affectation. It has been identified that ADCK2 gene is involved in CoQ biosynthesis and its mutation is responsible of a mitochondrial myopathy and liver dysfunction in humans. ADCK2 knockout mice in heterozygosis developed a skeletal muscle mitochondrial dysfunction and myopathy, liver steatosis and defects in oxidation of fatty acids under standard diet (ST). To understand the role of lipids in its phenotype, we have studied the consequences of a high fat diet (HFD) in ADCK2 knockout mice. Wild type (WT) or ADCK2 knockout were assigned to either ST or HFD for seven months (WT-ST n=5, WTHFD n=6, +/- ADCK2-ST n=4, +/- ADCK2-HFD n=4) and weights were obtained. Animals were housed individually to control weekly food ingestion. Ratio kilocalories ingested per gram of body mass (BM) was determined. Rectal body temperature was explored. Strength and running performance were investigated. Western blots and RT-PCR were performed. Descriptive statics and one-way ANOVA analyses were used. WT animals presented a higher weight than mutants after 31 weeks of study (WT: 31.16g vs. ADCK2 KO: 27.55g in ST and WT: 43.47g vs. ADCK2 KO: 35.20g in HFD; p<0.05). Weight gain significantly differed between the genotype and diets (WT: 2.00g vs. ADCK2: 2.50g in ST and WT: 14.43g vs. ADCK2: 9.55g in HFD; p<0.05). There were no significant differences in kilocalorie intake among mice in the same diet independently of their genotype. Mutants in HFD presented a higher ratio kilocalorie ingested per gram of BM (p<0.05), they tend to exhibit higher body temperature. This group showed higher levels of mRNA and protein of UCP1 in brown adipose tissue, UCP2 in liver and UCP3 in quadriceps, proteins involved in dissipation of energy as heat. ADCK2 KO showed significantly higher insulin resistance on HFD (p<0.05) than control, and also showed decreased strength and running performance. MEFs from ADCK2 KO mice showed dysfunctional respiration by fatty acids as bioenergetics substrate. ADCK2 KO showed a defective fat accumulation under HFD due to decreased weight gain associated to higher rectal temperature, which is apparently due to upregulation of UCPs proteins. These results support the role of ADCK2 encoded protein in mitochondria oxidation of fatty acids and lipid metabolism. As skeletal muscle functions highly depend on fatty acids, our results support the decrease of strength and running performance of ADCK2 KO in HFD.
DescriptionPóster presentado al Joint Congress of the Spanish Societies of Genetics, Cell Biology and Developmental Biology, celebrado en Gijón del 24 al 27 de octubre de 2017.
Appears in Collections:(CABD) Comunicaciones congresos
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