Prevention of diet-induced obesity by safflower oil: insights at the levels of PPAR , Orexin, and Ghrelin gene expression of adipocytes in mice

AbstractPaternal obesity is known to have a negative impact on the male’s reproductive health as well as the health of his offspring. Although epigenetic mechanisms have been implicated in the non-genetic transmission of acquired traits, the effect of paternal obesity on gene expression in the preimplantation embryo has not been fully studied. To this end, we investigated whether paternal obesity is associated with gene expression changes in eight-cell stage embryos fathered by males on a high-fat diet. We used single embryo RNA-seq to compare the gene expression profile of embryos generated by males on a high fat (HFD) versus control (CD) diet. This analysis revealed significant upregulation of the Samd4b and Gata6 gene in embryos in response to a paternal HFD. Furthermore, we could show a significant increase in expression of both Gata6 and Samd4b during differentiation of stromal vascular cells into mature adipocytes. These findings suggest that paternal obesity may induce changes in the male germ cells which are associated with the gene expression changes in the resulting preimplantation embryos.

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Ghrelin Gene Expression in Broiler Proventriculus Tissue are Changed by Feed Restriction, Different Dietary Energy and Protein Levels

American Journal of Animal and Veterinary Sciences ◽

10.3844/ajavsp.2010.175.179 ◽

2010 ◽

Vol 5 (3) ◽

pp. 175-179 ◽

Cited By ~ 1

Author(s):

Shokoufe Ghazanfari ◽

Mohammad Reza Nassiry ◽

Mojtaba Tahmooresp ◽

Abdolreza Salehi ◽

Karim Nobari

Keyword(s):

Gene Expression ◽

Feed Restriction ◽

Dietary Energy ◽

Protein Levels ◽

Ghrelin Gene

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Diet-Induced Obesity Disrupts Trace Element Homeostasis and Gene Expression in the Olfactory Bulb

Nutrients ◽

10.3390/nu12123909 ◽

2020 ◽

Vol 12 (12) ◽

pp. 3909

Author(s):

Melissa S. Totten ◽

Derek M. Pierce ◽

Keith M. Erikson

Keyword(s):

Gene Expression ◽

Olfactory Bulb ◽

Trace Element ◽

Alpha Synuclein ◽

Divalent Metal Transporter 1 ◽

Diet Induced Obesity ◽

Mrna Gene ◽

The Impact ◽

Mrna Gene Expression ◽

Obese Male

The aim of this study was to determine the impact of diet-induced obesity (DIO) on trace element homeostasis and gene expression in the olfactory bulb and to identify potential interaction effects between diet, sex, and strain. Our study is based on evidence that obesity and olfactory bulb impairments are linked to neurodegenerative processes. Briefly, C57BL/6J (B6J) and DBA/2J (D2J) male and female mice were fed either a low-fat diet or a high-fat diet for 16 weeks. Brain tissue was then evaluated for iron, manganese, copper, and zinc concentrations and mRNA gene expression. There was a statistically significant diet-by-sex interaction for iron and a three-way interaction between diet, sex, and strain for zinc in the olfactory bulb. Obese male B6J mice had a striking 75% increase in iron and a 50% increase in manganese compared with the control. There was an increase in zinc due to DIO in B6J males and D2J females, but a decrease in zinc in B6J females and D2J males. Obese male D2J mice had significantly upregulated mRNA gene expression for divalent metal transporter 1, alpha-synuclein, amyloid precursor protein, dopamine receptor D2, and tyrosine hydroxylase. B6J females with DIO had significantly upregulated brain-derived neurotrophic factor expression. Our results demonstrate that DIO has the potential to disrupt trace element homeostasis and mRNA gene expression in the olfactory bulb, with effects that depend on sex and genetics. We found that DIO led to alterations in iron and manganese predominantly in male B6J mice, and gene expression dysregulation mainly in male D2J mice. These results have important implications for health outcomes related to obesity with possible connections to neurodegenerative disease.

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The anorexigenic cytokine ciliary neurotrophic factor stimulates POMC gene expression via receptors localized in the nucleus of arcuate neurons

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00388.2011 ◽

2012 ◽

Vol 302 (4) ◽

pp. E458-E467 ◽

Cited By ~ 9

Author(s):

Odile Couvreur ◽

Alain Aubourg ◽

Delphine Crépin ◽

Jéril Degrouard ◽

Arieh Gertler ◽

...

Keyword(s):

Gene Expression ◽

Cell Nucleus ◽

Neurotrophic Factor ◽

Energy Homeostasis ◽

Ciliary Neurotrophic Factor ◽

Hypothalamic Region ◽

Diet Induced Obesity ◽

Food Intake Regulation ◽

Pomc Gene ◽

Intake Regulation

Ciliary neurotrophic factor (CNTF) is a neural cytokine that reduces appetite and body weight when administrated to rodents or humans. We have demonstrated recently that the level of CNTF in the arcuate nucleus (ARC), a key hypothalamic region involved in food intake regulation, is positively correlated with protection against diet-induced obesity. However, the comprehension of the physiological significance of neural CNTF action was still incomplete because CNTF lacks a signal peptide and thus may not be secreted by the classical exocytosis pathways. Knowing that CNTF distribution shares similarities with that of its receptor subunits in the rat ARC, we hypothesized that CNTF could exert a direct intracrine effect in ARC cells. Here, we demonstrate that CNTF, together with its receptor subunits, translocates to the cell nucleus of anorexigenic POMC neurons in the rat ARC. Furthermore, the stimulation of hypothalamic nuclear fractions with CNTF induces the phosphorylation of several signaling proteins, including Akt, as well as the transcription of the POMC gene. These data strongly suggest that intracellular CNTF may directly modulate POMC gene expression via the activation of receptors localized in the cell nucleus, providing a novel plausible mechanism of CNTF action in regulating energy homeostasis.

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Renal Mitochondrial Gene Expression is Dependent on Time of Day in Diet‐induced Obesity

The FASEB Journal ◽

10.1096/fasebj.2021.35.s1.04360 ◽

2021 ◽

Vol 35 (S1) ◽

Author(s):

Jazmine Benjamin ◽

Jackson Colson ◽

Dingguo Zhang ◽

David Pollock

Keyword(s):

Gene Expression ◽

Mitochondrial Gene ◽

Time Of Day ◽

Mitochondrial Gene Expression ◽

Diet Induced Obesity

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Abstract 63: ACE2 Deficiency Reduces Insulin Content of Isolated Pancreatic Islets and Plasma Insulin Concentrations Post-Glucose Challenge in Obese C57BL/6 Mice

Hypertension ◽

10.1161/hyp.62.suppl_1.a63 ◽

2013 ◽

Vol 62 (suppl_1) ◽

Author(s):

Robin C Shoemaker ◽

Lisa A Cassis

Keyword(s):

Gene Expression ◽

Insulin Secretion ◽

Pancreatic Islets ◽

Plasma Insulin ◽

Insulin Content ◽

Isolated Pancreatic Islets ◽

Diet Induced Obesity ◽

Glucose Challenge ◽

Ace2 Gene ◽

Deficient Mice

Objective: Diet-induced obesity promotes type 2 diabetes (T2D). Drugs that inhibit the renin-angiotensin system (RAS) have been demonstrated in clinical trials to decrease the onset of T2D. Angiotensin converting enzyme 2 (ACE2) negatively regulates the RAS by catabolizing angiotensin II (AngII). Preliminary data indicate that ACE2 deficient mice display impairments in glucose homeostasis at 8 weeks of age. We tested the hypothesis that ACE2 deficiency promotes the development of glucose intolerance and β-cell dysfunction in mice with diet-induced obesity. Methods and Results: Male Ace2 +/y or -/y mice were fed a low fat (LF, 10% kcal as fat) or high fat (HF, 60% kcal as fat) diet for 5 or 17 weeks. After 5 weeks, plasma insulin concentrations (0, 30 min) following a glucose challenge were significantly greater in HF versus ( vs) LF-fed mice. However, glucose-stimulated increases in plasma insulin concentrations were decreased in HF-fed ACE2 deficient mice compared to controls (2.96 ± 0.18 vs 4.44 ± 0.40 ng/ul, respectively; P<0.01). Surprisingly, isolated pancreatic islets from HF-fed mice of either genotype released similar concentrations of insulin in response to glucose. However, mRNA abundance of insulin was significantly reduced in islets from HF-fed Ace2 -/y compared to +/y mice (1.76 ± 0.17 vs 2.54 ± 0.18 insulin/18S ratio; P<0.05). After 17 weeks, the plasma insulin response to glucose was further reduced in the HF-fed ACE2 deficient mice compared to controls (8.07 ± 0.98 vs 13.90 ± 1.10 ng/ul; P<0.01). Further, LF-fed ACE2 deficient mice also displayed reductions in plasma glucose-stimulated insulin concentrations (1.92 ± 0.98 vs 3.09 ± 0.98 ng/ul; P<0.01). Islets from HF-fed wild type mice displayed reduced ACE2 gene expression compared to LF (0.069 ± 0.009 vs 0.169 ± 0.01, ACE2/18S ratio; P<0.001) and AngII totally suppressed islet glucose-stimulated insulin secretion compared to vehicle (-0.16 ± 0.18 vs 0.9 ± 0.26, fold change over basal; P<0.05). Conclusions: These results demonstrate that ACE2 deficiency promotes the development of T2D by regulating islet insulin content. Moreover, diet-induced obesity reduces islet ACE2 gene expression with augmented AngII-induced impairment of insulin secretion.

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