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Nutrients ; 10(12)2018 Dec 15.
Article in English | MEDLINE | ID: mdl-30558306

ABSTRACT

Diabetes and the related disease metabolic syndrome are epidemic in the United States, in part due to a shift in diet and decrease in physical exercise. PAS kinase is a sensory protein kinase associated with many of the phenotypes of these diseases, including hepatic triglyceride accumulation and metabolic dysregulation in male mice placed on a high-fat diet. Herein we provide the first characterization of the effects of western diet (high-fat high-sugar, HFHS) on Per-Arnt-Sim kinase mice (PASK-/-) and the first characterization of both male and female PASK-/- mice. Soleus muscle from the PASK-/- male mice displayed a 2-fold higher oxidative phosphorylation capacity than wild type (WT) on the normal chow diet. PASK-/- male mice were also resistant to hepatic triglyceride accumulation on the HFHS diet, displaying a 2.7-fold reduction in hepatic triglycerides compared to WT mice on the HFHS diet. These effects on male hepatic triglyceride were further explored through mass spectrometry-based lipidomics. The absence of PAS kinase was found to affect many of the 44 triglycerides analyzed, preventing hepatic triglyceride accumulation in response to the HFHS diet. In contrast, the female mice showed resistance to hepatic triglyceride accumulation on the HFHS diet regardless of genotype, suggesting the effects of PAS kinase may be masked.


Subject(s)
Cell Respiration , Diet, Western , Dietary Fats/adverse effects , Dietary Sugars/adverse effects , Liver/metabolism , Protein Serine-Threonine Kinases/metabolism , Triglycerides/blood , Animals , Aryl Hydrocarbon Receptor Nuclear Translocator/metabolism , Basic Helix-Loop-Helix Transcription Factors/metabolism , Diabetes Mellitus/metabolism , Diet , Diet, High-Fat , Dietary Fats/administration & dosage , Dietary Fats/metabolism , Dietary Sugars/administration & dosage , Female , Genotype , Male , Mice, Inbred C57BL , Mice, Knockout , Muscle, Skeletal/metabolism , Protein Serine-Threonine Kinases/deficiency , Protein Serine-Threonine Kinases/genetics , Repressor Proteins/metabolism
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