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Discordant Fasting Signaling Response in Hearts of Mice with Diet-Induced Obeisity and Insulin Resistance

ABSTRACT: Sixteen mouse heart samples were analyzed in four groups: Normal, 24hr fast, Diet-Induced Obesity, and DIO with 24hr fast. The cytoplasmic fractions of IN-Sequence heart preparations (solubilized proteins excluding most myofilaments) were analyzed by Liquid Chromatography coupled Mass Spectrometry.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Joel Kooren

LAB HEAD: Jennifer Van Eyk

PROVIDER: PXD003345 | Pride | 2018-10-26

REPOSITORIES: Pride

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			Action	DRS
	JK_150428_Elite_fvbn10_Cyto.mzXML	Mzxml
	JK_150428_Elite_fvbn10_Cyto.pep.xml	Pepxml
	JK_150428_Elite_fvbn13_Cyto.mzXML	Mzxml
	JK_150428_Elite_fvbn13_Cyto.pep.xml	Pepxml
	JK_150428_Elite_fvbn14_Cyto.mzXML	Mzxml

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Publications

Discordant signaling and autophagy response to fasting in hearts of obese mice: Implications for ischemia tolerance.

Andres Allen M AM Kooren Joel A JA Parker Sarah J SJ Tucker Kyle C KC Ravindran Nandini N Ito Bruce R BR Huang Chengqun C Venkatraman Vidya V Van Eyk Jennifer E JE Gottlieb Roberta A RA Mentzer Robert M RM

American journal of physiology. Heart and circulatory physiology 20160506 1

Autophagy is regulated by nutrient and energy status and plays an adaptive role during nutrient deprivation and ischemic stress. Metabolic syndrome (MetS) is a hypernutritive state characterized by obesity, dyslipidemia, elevated fasting blood glucose levels, and insulin resistance. It has also been associated with impaired autophagic flux and larger-sized infarcts. We hypothesized that diet-induced obesity (DIO) affects nutrient sensing, explaining the observed cardiac impaired autophagy. We su ...[more]

PMID: 27199111

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Requirement of hepatic pyruvate carboxylase during fasting, high fat and ketogenic diet

Project description:Pyruvate has two major fates upon entry into mitochondria, the oxidative decarboxylation to acetyl-CoA or the biotin-dependent carboxylation to oxaloacetate via pyruvate carboxylase (Pcx). Here we have generated mice with a liver specific knockout of pyruvate carboxylase (PcxL-/-) to understand the role of Pcx in hepatic mitochondrial metabolism under disparate physiological states. PcxL-/- mice exhibited a deficit in hepatic gluconeogenesis as expected but were able to maintain systemic euglycemia following a 24hr fast and enhanced ketogenesis. Feeding a high fat diet to PcxL-/- mice resulted in animals that were resistant to glucose intolerance without affecting body weight. However, PcxL-/- mice fed a ketogenic diet for 1 week became severely hypoglycemic, demonstrating a requirement for hepatic Pcx for long term glycemia under carbohydrate limited diets. Loss of Pcx was associated with an induction of protein acetylation in PcxL-/- mice regardless of physiologic state. Furthermore, liver acetyl-proteomics revealed a biased induction in mitochondrial lysine acetylation. These data show that Pcx is important for maintaining the proper balance of pyruvate metabolism between oxidative and anaplerotic pathways.

2022-10-31 | PXD032028 | Pride

Fasting does not promote a metabolic memory effect in mouse liver

Project description:Background: Tissues may respond differently to a particular stimulus if they have been previously exposed to that same stimulus. Here we tested the hypothesis that a strong metabolic stimulus may elicit a memory effect in the liver. To that end, we examined whether prior fasting, which profoundly impacts hepatic nutrient metabolism, may influence the metabolic response to a subsequent fast. Methods: 24 mice were exposed to two 16h fasts over a 8 week period, each time being allowed to return to their normal growth trajectory, while another group of 24 mice was fed ad libitum throughout. Of each group, half of the mice were euthanized after a 16h fast, whereas the other half was euthanized in the ab libitum fed state. Results: An acute fast significantly increased plasma NEFA, glycerol, β-hydroxybutyrate and liver triglycerides, and decreased plasma glucose, triglycerides, and liver glycogen levels. An acute fast also markedly changed the liver transcriptome, upregulating genes involved in fatty acid catabolism and downregulating genes involved in cholesterol synthesis, and majorly impacted the liver metabolome, reducing the levels of numerous amino acids, glycolysis and TCA cycle intermediates, and nucleotides. However, none of the these changes were significantly influenced by prior fasting. The limited number of genes that were significantly altered by prior fasting are likely false positives. Finally, no significant effect was observed of prior fasting on glucose tolerance. Conclusion: We conclude that previous exposure to fasting in mice does not influence the metabolic response to a subsequent fast, thus arguing against the concept of metabolic memory in the hepatic response to fasting.

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