ZBTB16 and Metabolic Syndrome: a Network Perspective

Seda, O.; Šedová, Lucie; Včelák, Josef; Vaňková, Markéta; Liška, František; Bendlová, Běla

doi:10.33549/physiolres.933730

Cited by 34 publications

(23 citation statements)

References 55 publications

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“…Strains used in this study differed in a single gene mutation-254 kb deletion in intronic region of Zbtb16 gene of the PD/Cub strain origin [37]. The genomic background of SHR was thought to exacerbate the effects of Zbtb16 gene involved in pathogenesis of metabolic syndrome [18], but conversely was shown to improve the related parameters [20], which was to an extent apparent in our study as well.…”

Section: Discussionsupporting

confidence: 57%

“…In addition to alternative carbohydrate source in maternal diet we introduced a small genetic difference in Zbtb16 (Zbtb16-Zinc Finger and BTB Domain Containing 16) gene between animals in the study design. Recent studies show that Zbtb16 acts as a pleiotropic factor involved in embryogenesis, cell differentiation and lipid and glucose metabolism [18]. We and others previously established the importance of Zbtb16 gene in metabolic syndrome and its nutrigenetic aspects [18][19][20].…”

Section: Introductionmentioning

confidence: 90%

“…Recent studies show that Zbtb16 acts as a pleiotropic factor involved in embryogenesis, cell differentiation and lipid and glucose metabolism [18]. We and others previously established the importance of Zbtb16 gene in metabolic syndrome and its nutrigenetic aspects [18][19][20]. In particular, Zbtb16 targeted models of mice [19] and rats [20] show significantly reduced levels of triacylglycerols and cholesterol and exhibited lower levels of serum insulin and significantly increased sensitivity of adipose and muscle tissue to insulin action, respectively.…”

Section: Introductionmentioning

confidence: 98%

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Grandmother’s Diet Matters: Early Life Programming with Sucrose Influences Metabolic and Lipid Parameters in Second Generation of Rats

2020

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Early life exposure to certain environmental stimuli is related to the development of alternative phenotypes in mammals. A number of these phenotypes are related to an increased risk of disease later in life, creating a massive healthcare burden. With recent focus on the determination of underlying causes of common metabolic disorders, parental nutrition is of great interest, mainly due to a global shift towards a Western-type diet. Recent studies focusing on the increase of food or macronutrient intake don’t always consider the source of these nutrients as an important factor. In our study, we concentrate on the effects of high-sucrose diet, which provides carbohydrates in form of sucrose as opposed to starch in standard diet, fed in pregnancy and lactation in two subsequent generations of spontaneously hypertensive rats (SHR) and congenic SHR-Zbtb16 rats. Maternal sucrose intake increased fasting glycaemia in SHR female offspring in adulthood and increased their chow consumption in gravidity. High-sucrose diet fed to the maternal grandmother increased brown fat weight and HDL cholesterol levels in adult male offspring of both strains, i.e., the grandsons. Fasting glycaemia was however decreased only in SHR offspring. In conclusion, we show the second-generation effects of maternal exposition to a high-sucrose diet, some modulated to a certain extent by variation in the Zbtb16 gene.

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Section: Discussionsupporting

confidence: 57%

Section: Introductionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 98%

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Grandmother’s Diet Matters: Early Life Programming with Sucrose Influences Metabolic and Lipid Parameters in Second Generation of Rats

2020

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“…ZBTB16 encodes a transcription factor, which contains a BTB/POZ protein-protein interaction domain in its N-terminal and a C2H2-type zinc finger DNA binding domain in its C-terminal, playing key roles in many biological processes such as stem cell maintenance and proliferation, cell differentiation, spermatogenesis, musculoskeletal development, hematopoiesis, apoptosis, chromatin remodeling, metabolism and immunity 15,16 . A variant translocation in the ZBTB16 was first identified in a patient with acute promyelocytic leukemia 17 .…”

Section: Introductionmentioning

confidence: 99%

Zbtb16regulates social cognitive behaviors and neocortical development

Usui

Berto

Konishi

et al. 2020

Preprint

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Recent genetic studies have underscored the pleiotropic effects of single genes to multiple cognitive disorders. Mutations of ZBTB16 are associated with autism spectrum disorder (ASD) and schizophrenia (SCZ), but how the function of ZBTB16 is related to ASD or SCZ remains unknown. Here we show the deletion of Zbtb16 in mice leads to both ASD- and SCZ-like behaviors such as social impairment, repetitive behaviors, risk-taking behaviors, and cognitive impairment. To elucidate the mechanism underlying the behavioral phenotypes, we carried out histological studies and observed impairments in thinning of neocortical layer 6 (L6) and a reduction of TBR1+ neurons in the prefrontal cortex (PFC) of Zbtb16 KO mice. Furthermore, we found increased dendritic spines and microglia as well as developmental defects in oligodendrocytes and neocortical myelination in the PFC of Zbtb16 KO mice. Using a genomics approach, we identified the Zbtb16-transcriptome that includes genes involved in both ASD and SCZ pathophysiology and neocortical maturation such as neurogenesis and myelination. Co-expression networks further identified Zbtb16-correlated modules that are unique to ASD or SCZ respectively. Our study provides insight into the differential role of ZBTB16 in ASD and SCZ.

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“…Our previous sequence analysis revealed a conservative amino acid substitution (T208S) and a 2,964-bp deletion in intron 2 of PD/Cub’s Zbtb16 gene ( 19 ). Zbtb16 is a pleiotropic transcription factor involved, among others, in processes underlying pathogenesis of practically all major constituents of metabolic syndrome, as reviewed recently ( 20 ). In this study, we created two new models, one of them carrying only the Zbtb16 gene from the original segment to retest its effect on DEX-induced metabolic syndrome features by comparing their metabolic profiles including global and tissue-specific insulin sensitivity.…”

Section: Introductionmentioning

confidence: 99%

Single-Gene Congenic Strain Reveals the Effect of Zbtb16 on Dexamethasone-Induced Insulin Resistance

et al. 2018

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BackgroundGlucocorticoids (GCs) are potent therapeutic agents frequently used for treatment of number of conditions, including hematologic, inflammatory, and allergic diseases. Both their therapeutic and adverse effects display significant interindividual variation, partially attributable to genetic factors. We have previously isolated a seven-gene region of rat chromosome 8 sensitizing to dexamethasone (DEX)-induced dyslipidemia and insulin resistance (IR) of skeletal muscle. Using two newly derived congenic strains, we aimed to investigate the effect of one of the prime candidates for this pharmacogenetic interaction, the Zbtb16 gene.MethodsAdult male rats of SHR-Lx.PD5PD-Zbtb16 (n = 9) and SHR-Lx.PD5SHR-Zbtb16 (n = 8) were fed standard diet (STD) and subsequently treated with DEX in drinking water (2.6 µg/ml) for 3 days. The morphometric and metabolic profiles of both strains including oral glucose tolerance test, triacylglycerols (TGs), free fatty acids, insulin, and C-reactive protein levels were assessed before and after the DEX treatment. Insulin sensitivity of skeletal muscle and visceral adipose tissue was determined by incorporation of radioactively labeled glucose.ResultsThe differential segment of SHR-Lx.PD5SHR-Zbtb16 rat strain spans 563 kb and contains six genes: Htr3a, Htr3b, Usp28, Zw10, Tmprss5, and part of Drd2. The SHR-Lx.PD5PD-Zbtb16 minimal congenic strain contains only Zbtb16 gene on SHR genomic background and its differential segment spans 254 kb. Total body weight was significantly increased in SHR-Lx.PD5PD-Zbtb16 strain compared with SHR-Lx.PD5SHR-Zbtb16, however, no differences in the weights of adipose tissue depots were observed. While STD-fed rats of both strains did not show major differences in their metabolic profiles, after DEX treatment the SHR-Lx.PD5PD-Zbtb16 congenic strain showed increased levels of TGs, glucose, and blunted inhibition of lipolysis by insulin. Both basal and insulin-stimulated incorporation of radioactively labeled glucose into skeletal muscle glycogen were significantly reduced in SHR-Lx.PD5PD-Zbtb16 strain, but the insulin sensitivity of adipose tissue was comparable between the two strains.ConclusionThe metabolic disturbances including impaired glucose tolerance, dyslipidemia, and IR of skeletal muscle observed after DEX treatment in the congenic SHR-Lx.PD5PD-Zbtb16 reveal the Zbtb16 locus as a possible sensitizing factor for side effects of GC therapy.

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ZBTB16 and Metabolic Syndrome: a Network Perspective

Cited by 34 publications

References 55 publications

Grandmother’s Diet Matters: Early Life Programming with Sucrose Influences Metabolic and Lipid Parameters in Second Generation of Rats

Grandmother’s Diet Matters: Early Life Programming with Sucrose Influences Metabolic and Lipid Parameters in Second Generation of Rats

Zbtb16regulates social cognitive behaviors and neocortical development

Single-Gene Congenic Strain Reveals the Effect of Zbtb16 on Dexamethasone-Induced Insulin Resistance

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