Feeding induced changes in the hypothalamic transcriptome

Giorgio, Maria Rita De; Yoshioka, Mayumi; St‐Amand, Jonny

doi:10.1016/j.cca.2009.06.004

Cited by 19 publications

(23 citation statements)

References 40 publications

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“…However, without any calorie increase, it is plausible that the introduction of specific dietary components in solid foods or resultant alterations in gut flora may result in epigenetic modification of metabolic programming, as shown in rodent models. [23][24][25][26] These early feeding-related changes may have lifelong detrimental effects. Other hypotheses relate to specific nutrients, for example excess protein intake in infancy may increase insulin-like growth factor-1 levels, leading to increased differentiation of preadipocytes into adipocytes, and leading to earlier age at adiposity rebound.…”

Section: Discussionmentioning

confidence: 99%

Delayed introduction of solid feeding reduces child overweight and obesity at 10 years

et al. 2010

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Section: Discussionmentioning

confidence: 99%

Delayed introduction of solid feeding reduces child overweight and obesity at 10 years

et al. 2010

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“…Urinary MUPs mediate chemical signaling in conspecifics (Tirindelli et al, 2009). The MUP family members are also expressed in the submaxillary, lachrymal, nasal, parotid, mammary glands, and hypothalami; however, the function of extrahepatic MUPs is unknown (Cavaggioni and Mucignat-Caretta, 2000; De Giorgio et al, 2009; Shaw et al, 1983). …”

Section: Mup Protein Structure and Polymorphismmentioning

confidence: 99%

“…Two groups reported independently that hepatic MUP1 expression and circulating MUP1 levels are markedly reduced in mice with either genetic (leptin receptor-deficient db/db ) or dietary fat-induced obesity (Hui et al, 2009; Zhou et al, 2009). Interestingly, MUP1 is also expressed in several extrahepatic tissues, and MUP1 expression is similarly reduced in both adipose tissues and the hypothalamus in response to nutrient deprivation (De Giorgio et al, 2009; van Schothorst et al, 2006). Adipocytes and hypothalamic neurons are also key players in nutrient sensing.…”

Section: Mup Regulation Of Nutrient Metabolismmentioning

confidence: 99%

“…Therefore, MUP1 may also regulate hepatic glucose and lipid metabolism in an autocrine and/or paracrine fashion. Interestingly, MUP1 expression is also regulated by nutrients in adipose tissue and the hypothalamus, suggesting that MUP1 may regulate the metabolic activity of these two tissues in a similar autocrine and/or paracrine manner (De Giorgio et al, 2009; van Schothorst et al, 2006). …”

Section: Mup Regulation Of Nutrient Metabolismmentioning

confidence: 99%

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Major Urinary Protein Regulation of Chemical Communication and Nutrient Metabolism

Zhou

Rui

2010

Vitamins &Amp; Hormones

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Summary The major urinary protein (MUP) family members contain a conserved β-barrel structure with a characteristic central hydrophobic pocket. They are secreted by the liver and excreted into the urine. MUPs bind via their central pockets to volatile pheromones or other lipophilic molecules, and regulate pheromone transportation in the circulation, excretion in the kidney, and release into the air from urine marks. MUPs are highly polymorphic, and the MUP profiles in urine function as individual identity signatures of the owners. The MUP signatures are detected by the main and accessory olfactory systems and trigger adaptive behavioral responses and/or developmental processes. Circulating MUPs serve as a metabolic signal to regulate glucose and lipid metabolism. Recombinant MUP1 markedly ameliorates hyperglycemia and glucose intolerance in mice with type 2 diabetes. MUP1 suppresses hepatic gluconeogenesis and promotes energy expenditure in skeletal muscle by stimulating mitochondrial biogenesis and function. MUPs are unique members of the lipocalin super-family that mediate both chemical and metabolic signaling.

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“…In addition, 5 potentially novel transcripts were differentially modulated. So, these authors identified genes that may regulate hypothalamic circuits governing the early response to food intake 3 genes were specifically modulated by high-fat intake [28]. Makedonski et al (2005) hypothesize that part of the Rett syndrome (RS), a neurodevelopmental disorder, phenotype is due to MeCP2-associated silencing of UBE3A.…”

mentioning

confidence: 99%

Leptin Signaling Modulates Expression of Polycomb and Trithorax Complexes in the Brain of Fat Tissue Implanted Polycystic Ovarian Sindrome Mice

Freitas¹,

Noronha²,

Ritto³

et al. 2014

AJMB

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The Polycystic Ovary Syndrome (PCOS) is the most common androgenic disorder in women during reproductive life. PCOS may also be accompanied by metabolic syndrome and recent studies point to leptin as playing a role in disrupting infertility and in changing the energy balance in obese mice through its action on the hypothalamus. The aim is to assess the expression of the Polycomb & Trithorax Complexes genes in brain of mice transplanted with fat tissue from normal mice, in order to better understand the neuronal mechanisms underlying the reversion of PCOS. Three B6 V-Lepob/J mouse groups: Normal weight, obese and seven-day-treatment obese had their brain RNA extracted and submitted to an 84 Polycomb & Trithorax Complexes genes PCR Array plate and Metacore TM pathways localization. Genomic profiles obtained were compared to the ones of the normal-weight-mice group. Differentially expressed genes were 13% and 26% respectively to control and treatment. Major changes were in genes: Snai1/31; Smarca1/−17; Dnmt3b/4.7; Ezh1/ 15. Altered genes were associated to canonical pathways and provided 3 networks related to epi-* Corresponding author. E. H. da Silva Freitas et al. 178genetics. Underlying neuronal changes caused by leptin in obese mice brain, there is an important role being played by the histone code. Here there is evidence that leptin drives the chromatin packing to a more condensed pattern. Upregulation of methyltransferase genes, like Ezh1, favors this thought. In summary the Polycomb & Trithorax complexes might answer for the silencing of some downregulated genes in the obese mice brain when exposed to leptin.

show abstract

Feeding induced changes in the hypothalamic transcriptome

Cited by 19 publications

References 40 publications

Delayed introduction of solid feeding reduces child overweight and obesity at 10 years

Delayed introduction of solid feeding reduces child overweight and obesity at 10 years

Major Urinary Protein Regulation of Chemical Communication and Nutrient Metabolism

Leptin Signaling Modulates Expression of Polycomb and Trithorax Complexes in the Brain of Fat Tissue Implanted Polycystic Ovarian Sindrome Mice

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