Dataset Information

Identification of microRNAs controlling hepatic mRNA levels for metabolic genes during the metabolic transition from embryonic to posthatch development in the chicken.

ABSTRACT: The transition from embryonic to posthatch development in the chicken represents a massive metabolic switch from primarily lipolytic to primarily lipogenic metabolism. This metabolic switch is essential for the chick to successfully transition from the metabolism of stored egg yolk to the utilization of carbohydrate-based feed. However, regulation of this metabolic switch is not well understood. We hypothesized that microRNAs (miRNAs) play an important role in the metabolic switch that is essential to efficient growth of chickens. We used high-throughput RNA sequencing to characterize expression profiles of mRNA and miRNA in liver during late embryonic and early posthatch development of the chicken. This extensive data set was used to define the contributions of microRNAs to the metabolic switch during development that is critical to growth and nutrient utilization in chickens.We found that expression of over 800 mRNAs and 30 miRNAs was altered in the embryonic liver between embryonic day 18 and posthatch day 3, and many of these differentially expressed mRNAs and miRNAs are associated with metabolic processes. We confirmed the regulation of some of these mRNAs by miRNAs expressed in a reciprocal pattern using luciferase reporter assays. Finally, through the use of yeast one-hybrid screens, we identified several proteins that likely regulate expression of one of these important miRNAs.Integration of the upstream regulatory mechanisms governing miRNA expression along with monitoring the downstream effects of this expression will ultimately allow for the construction of complete miRNA regulatory networks associated with the hepatic metabolic switch in chickens. Our findings support a key role for miRNAs in controlling the metabolic switch that occurs between embryonic and posthatch development in the chicken.

SUBMITTER: Hicks JA

PROVIDER: S-EPMC5583987 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

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Identification of microRNAs controlling hepatic mRNA levels for metabolic genes during the metabolic transition from embryonic to posthatch development in the chicken.

Hicks Julie A JA Porter Tom E TE Liu Hsiao-Ching HC

BMC genomics 20170905 1

<h4>Background</h4>The transition from embryonic to posthatch development in the chicken represents a massive metabolic switch from primarily lipolytic to primarily lipogenic metabolism. This metabolic switch is essential for the chick to successfully transition from the metabolism of stored egg yolk to the utilization of carbohydrate-based feed. However, regulation of this metabolic switch is not well understood. We hypothesized that microRNAs (miRNAs) play an important role in the metabolic sw ...[more]

PMID: 28870167

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Project description:The liver is the main site of de novo lipogenesis in poultry, and hepatic lipid metabolism disorder will lead to excessive abdominal fat deposition or fatty liver disease, finally causing huge economic loss. The present study was conducted to investigate developmental changes in hepatic lipid metabolism of chicks from embryonic periods to the first week after hatching. Liver samples were collected from embryonic day 11 (E11) to the age of day 7 posthatch (D7) for lipid metabolism analysis. Hematoxylin-eosin and Oil Red O staining analysis showed that hepatic lipids increased gradually during embryonic period and declined posthatch; The sum of hepatic triglycerides and cholesterol reached the peak at E19 and D1 by ELISA analysis (P < 0.05). Acetyl-CoA carboxylase, fatty acid synthase, and acyl-CoA desaturase 1 mRNA expression in the liver were higher from E17 to D1 with the peak at E19 when compared with those at E13 and E15 (P < 0.05). Hepatic elongase of very long-chain fatty acids 6 and microsomal triglyceride transfer protein mRNA abundance were lower during embryonic periods but reached relative higher level after hatching (P < 0.05). On the contrary, hepatic carbohydrate response element binding protein (ChREBP), carnitine palmitoyltransferase 1, and peroxisome proliferators-activated receptor α expression were higher during embryonic periods but decreased posthatch (P < 0.05). The mRNA abundance of sterol-regulatory element binding protein 1c was the lowest at E13 and E15, then increased gradually from E17 to D1, while decreased from D3 to D7 little by little (P < 0.05). In summary, hepatic lipogenesis genes have different expression patterns during the embryonic periods and the first week of posthatch, which might be activated by ChREBP during embryonic periods; fatty acid oxidation was enhanced around the hatched day but declined posthatch. These findings will broaden the understanding of physiological characteristics and dynamic pattern about hepatic lipid metabolism in chicks.

Project description:ObjectiveThe mechanistic target of rapamycin (mTOR) is a serine/threonine kinase that functions into distinct protein complexes (mTORC1 and mTORC2) that regulates growth and metabolism. DEP-domain containing mTOR-interacting protein (DEPTOR) is part of these complexes and is known to reduce their activity. Whether DEPTOR loss affects metabolism and organismal growth in vivo has never been tested.MethodsWe have generated a conditional transgenic mouse allowing the tissue-specific deletion of DEPTOR. This model was crossed with CMV-cre mice or Albumin-cre mice to generate either whole-body or liver-specific DEPTOR knockout (KO) mice.ResultsWhole-body DEPTOR KO mice are viable, fertile, normal in size, and do not display any gross physical and metabolic abnormalities. To circumvent possible compensatory mechanisms linked to the early and systemic loss of DEPTOR, we have deleted DEPTOR specifically in the liver, a tissue in which DEPTOR protein is expressed and affected in response to mTOR activation. Liver-specific DEPTOR null mice showed a reduction in circulating glucose upon fasting versus control mice. This effect was not associated with change in hepatic gluconeogenesis potential but was linked to a sustained reduction in circulating glucose during insulin tolerance tests. In addition to the reduction in glycemia, liver-specific DEPTOR KO mice had reduced hepatic glycogen content when fasted. We showed that loss of DEPTOR cell-autonomously increased oxidative metabolism in hepatocytes, an effect associated with increased cytochrome c expression but independent of changes in mitochondrial content or in the expression of genes controlling oxidative metabolism. We found that liver-specific DEPTOR KO mice showed sustained mTORC1 activation upon fasting, and that acute treatment with rapamycin was sufficient to normalize glycemia in these mice.ConclusionWe propose a model in which hepatic DEPTOR accelerates the inhibition of mTORC1 during the transition to fasting to adjust metabolism to the nutritional status.

Dataset Information

Identification of microRNAs controlling hepatic mRNA levels for metabolic genes during the metabolic transition from embryonic to posthatch development in the chicken.

Publications

Identification of microRNAs controlling hepatic mRNA levels for metabolic genes during the metabolic transition from embryonic to posthatch development in the chicken.

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