Both prenatal and postnatal excessive consumption of dietary sucrose or fructose was shown to be detrimental to health and contributing to pathogenesis of metabolic syndrome. Our knowledge of genetic determinants of individual sensitivity to sucrose-driven metabolic effects is limited. In this study, we have tested the hypothesis that a variation of metabolic syndrome-related gene, Zbtb16 (Zinc Finger and BTB Domain Containing 16 will affect the reaction to high-sucrose diet (HSD) content in "matched" nutritional exposition settings, i.e. maternal HSD with re-exposition to HSD in adulthood vs. standard diet. We compared metabolic profiles of adult males of spontaneously hypertensive rats (SHR) and a single-gene, minimal congenic strain SHR-Zbtb16 fed either standard diet or exposed to HSD prenatally throughout gestation and nursing and again at the age of 6 months for the period of 14 days. HSD exposition led to increased adiposity in both strains and decrease of glucose tolerance and cholesterol (Ch) concentrations in majority of low-density lipoprotein (LDL) particle classes and in very large and large high-density lipoprotein (HDL) in SHR-Zbtb16 male offspring. There was a similar pattern of HSD-induced increase of triacylglycerols in chylomicrons and very low-density lipoprotein (VLDL) of both strains, though the increase of (triacylglycerol) TAG content was clearly more pronounced in SHR. We observed significant STRAIN*DIET interactions for the smallest LDL particles as their TAG content decreased in SHR-Zbtb16 and did not change in SHR in response to HSD. In summary, we provide evidence of nutrigenetic interaction between Zbtb16 and HSD in context of pathogenesis of metabolic syndrome.

• MeSH
• Cholesterol metabolism   MeSH
• Hypertension genetics   metabolism   MeSH
• Dietary Sucrose metabolism   MeSH
• Rats MeSH
• Metabolic Syndrome etiology   metabolism   pathology   MeSH
• Disease Models, Animal MeSH
• Nutrigenomics methods   MeSH
• Rats, Inbred SHR MeSH
• Promyelocytic Leukemia Zinc Finger Protein genetics   metabolism   MeSH
• Sweetening Agents metabolism   MeSH
• Pregnancy MeSH
• Triglycerides metabolism   MeSH
• Animals, Congenic MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Pregnancy MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Cholesterol MeSH
• Dietary Sucrose MeSH
• Promyelocytic Leukemia Zinc Finger Protein MeSH
• Sweetening Agents MeSH
• Triglycerides MeSH
• ZBTB16 protein, rat MeSH Browser

Metabolic interactions between adipose tissue and the heart may play an active role in progression of heart failure (HF). The aim of the study was to examine changes in myocardial and adipose tissue metabolism and gene expression in a rat HF model induced by chronic volume overload. HF was induced by volume overload from aorto-caval fistula (ACF) in 3-month-old male Wistar rats and animals were studied in the phase of decompensated HF (22nd week). HF rats showed marked eccentric cardiac hypertrophy, pulmonary congestion, increased LV end-diastolic pressure, and intraabdominal fat depletion. HF rats had preserved glucose tolerance, but increased circulating free fatty acids (FFA) and attenuated insulin response during oral glucose challenge. Isolated organ studies showed preserved responsiveness of adipose tissue lipolysis and lipogenesis to epinephrine and insulin in ACF. The heart of HF animals had markedly reduced triglyceride content (almost to half of controls), attenuated anti-oxidative reserve (GSH/GSSG), upregulated HF markers (ANP, periostin, thrombospondin-4), specific signaling pathways (Wnt, TGF-β), and downregulated enzymes of mitochondrial fatty acid oxidation, citric acid cycle, and respiratory chain. Adipose tissue transcription profiling showed upregulated receptor for gastric inhibitory polypeptide. In conclusion, ACF-induced HF model displays several deregulations of systemic metabolism. Despite elevation of systemic FFAs, myocardial triglycerides are low and insulin levels are attenuated, arguing against a role of lipotoxicity or insulin resistance in this model. Attenuated postprandial insulin response and relative lack of its antilipolytic effects may facilitate intraabdominal fat depletion observed in ACF-HF animals.

• MeSH
• Aorta surgery   MeSH
• Arteriovenous Fistula MeSH
• Arteriovenous Shunt, Surgical MeSH
• Biomarkers metabolism   MeSH
• Epididymis metabolism   pathology   MeSH
• Glucose Tolerance Test MeSH
• Glutathione metabolism   MeSH
• Hemodynamics MeSH
• Insulin blood   MeSH
• Liver pathology   MeSH
• Myocytes, Cardiac metabolism   pathology   MeSH
• Rats MeSH
• Fatty Acids, Nonesterified blood   MeSH
• Thiobarbituric Acid Reactive Substances metabolism   MeSH
• Kidney pathology   MeSH
• Lipid Metabolism MeSH
• Myocardium metabolism   pathology   MeSH
• Oxidative Stress MeSH
• Lung pathology   MeSH
• Rats, Wistar MeSH
• Ventricular Remodeling MeSH
• Heart physiopathology   MeSH
• Heart Failure metabolism   pathology   physiopathology   MeSH
• Gene Expression Profiling MeSH
• Superoxide Dismutase metabolism   MeSH
• Adipose Tissue metabolism   pathology   MeSH
• Organ Size MeSH
• Venae Cavae surgery   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Biomarkers MeSH
• Glutathione MeSH
• Insulin MeSH
• Fatty Acids, Nonesterified MeSH
• Thiobarbituric Acid Reactive Substances MeSH
• Superoxide Dismutase MeSH