Autophagy - Revision history

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2017-09-22T17:26:46Z

‎Ketones

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2017-09-17T18:24:40Z

‎Ketones

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2017-09-16T13:56:01Z

‎Ketones

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2017-09-16T13:51:41Z

‎Ketones

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2017-09-15T13:42:12Z

‎Ketones

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2017-09-15T13:36:15Z

‎Ketones

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2017-09-15T13:29:55Z

‎Ketones

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2017-09-15T13:29:31Z

‎Ketones

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2017-09-15T13:23:31Z

‎Ketones

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2017-09-14T18:35:52Z

‎Ketones

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 Energy-restricted metabolic states (CR, IF), extend lifespan in animals, not requiring overall reduced caloric intake [https://www.ncbi.nlm.nih.gov/pubmed/23598600/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491655/], but necessarily associated with elevations in ketone bodies. In starvation mode, when liver glycogen is depleted, the major source of fuel for the brains (and other tissues) shifts from glucose to ketone bodies (derived from fatty acids and ketogenic amino acids). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate. Levels of β-hydroxybutyrate increase dramatically on a ketogenic diet [https://www.ncbi.nlm.nih.gov/pubmed/18301085/], after 12–16 hours of fasting [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292859/][https://www.ncbi.nlm.nih.gov/pubmed/6986618/], and after 90 minutes of intense exercise [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1279383/].
-Thus elevated levels of ketones are conditionary to, and stimulate autophagy. Just as a small group of other metabolic intermediates that affect gene expression via chromatin modifications [https://www.ncbi.nlm.nih.gov/pubmed/22265398/], β-hydroxybutyrate (and butyrate[http://www.jbc.org/content/254/5/1716.long] competitively [https://www.ncbi.nlm.nih.gov/pubmed/18059533/], and at least four major structurally distinct classes[https://www.ncbi.nlm.nih.gov/pubmed/16955068/]) acts as an endogenous inhibitor of HDACs class 1 and 2a.[https://www.ncbi.nlm.nih.gov/pubmed/23223453/], which induces Foxo3a.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/] (Foxo3a is the mammalian ortholog of the stress-responsive transcriptional factor DAF16 that regulates lifespan in worms[https://www.ncbi.nlm.nih.gov/pubmed/20336132/])  Class I HDACs are associated with the regulation of lifespan in model organisms.[https://www.ncbi.nlm.nih.gov/pubmed/10512855/] βOHB delivered via the diet in the form of a synthetic ester improves learning and memory.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619192/]
+Thus elevated levels of ketones are conditionary to, and stimulate autophagy. Just as a small group of other metabolic intermediates that affect gene expression via chromatin modifications [https://www.ncbi.nlm.nih.gov/pubmed/22265398/], β-hydroxybutyrate (and butyrate[http://www.jbc.org/content/254/5/1716.long] competitively [https://www.ncbi.nlm.nih.gov/pubmed/18059533/], and at least four major structurally distinct classes[https://www.ncbi.nlm.nih.gov/pubmed/16955068/]) acts as an endogenous inhibitor of HDACs class 1 and 2a.[https://www.ncbi.nlm.nih.gov/pubmed/23223453/], which induces Foxo3a.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/] (Foxo3a is the mammalian ortholog of the stress-responsive transcriptional factor DAF16 that regulates lifespan in worms[https://www.ncbi.nlm.nih.gov/pubmed/20336132/])  Class I HDACs are associated with the regulation of lifespan in model organisms.[https://www.ncbi.nlm.nih.gov/pubmed/10512855/] Supplementary beta-hydroxybutyrate may maximally increase mean lifespan in C. elegans by 26%.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4169858/] βOHB delivered via the diet in the form of a synthetic ester improves learning and memory.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619192/]
 Ketogenic diets suppress fatty acid synthesis enzymes [https://www.ncbi.nlm.nih.gov/pubmed/17299079/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781352/] and strongly induce regulation of ketogenic genes, and one of its crucial downstream targets, resulting in increased transcription of ketogenic enzymes [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3119109/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781352/].

@@ Line 50: / Line 50: @@
 Ketogenic diets suppress fatty acid synthesis enzymes [https://www.ncbi.nlm.nih.gov/pubmed/17299079/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781352/] and strongly induce regulation of ketogenic genes, and one of its crucial downstream targets, resulting in increased transcription of ketogenic enzymes [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3119109/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781352/].
-A ketogenic diet also promotes mitochondrial biogenesis [https://www.ncbi.nlm.nih.gov/pubmed/20167576/] and increases expression of SIRT1 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821007/], which is also increased during calorie restriction and regulates a variety of aging-related pathways (reviewed in [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872805/])
+A ketogenic diet also promotes mitochondrial biogenesis [https://www.ncbi.nlm.nih.gov/pubmed/20167576/] and increases expression of SIRT1 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821007/], which is also increased during calorie restriction and regulates a variety of aging-related pathways (reviewed in [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872805/]) β-hydroxybutyrate does not extend lifespan in a setting of dietary restriction indicating that β-hydroxybutyrate is likely functioning through a similar mechanism.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4169858/]
 ==Antioxidants==

@@ Line 47: / Line 47: @@
 Energy-restricted metabolic states (CR, IF), extend lifespan in animals, not requiring overall reduced caloric intake [https://www.ncbi.nlm.nih.gov/pubmed/23598600/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491655/], but necessarily associated with elevations in ketone bodies. In starvation mode, when liver glycogen is depleted, the major source of fuel for the brains (and other tissues) shifts from glucose to ketone bodies (derived from fatty acids and ketogenic amino acids). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate. Levels of β-hydroxybutyrate increase dramatically on a ketogenic diet [https://www.ncbi.nlm.nih.gov/pubmed/18301085/], after 12–16 hours of fasting [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292859/][https://www.ncbi.nlm.nih.gov/pubmed/6986618/], and after 90 minutes of intense exercise [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1279383/].
-Thus elevated levels of ketones are conditionary to, and stimulate autophagy. Just as a small group of other metabolic intermediates that affect gene expression via chromatin modifications [https://www.ncbi.nlm.nih.gov/pubmed/22265398/], β-hydroxybutyrate (and butyrate[http://www.jbc.org/content/254/5/1716.long] competitively [https://www.ncbi.nlm.nih.gov/pubmed/18059533/], and at least four major structurally distinct classes[https://www.ncbi.nlm.nih.gov/pubmed/16955068/]) acts as an endogenous inhibitor of HDACs class 1 and 2a.[https://www.ncbi.nlm.nih.gov/pubmed/23223453/], which induces Foxo3a.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/] (Foxo3a is the mammalian ortholog of the stress-responsive transcriptional factor DAF16 that regulates lifespan in worms[https://www.ncbi.nlm.nih.gov/pubmed/20336132/])  Class I HDACs are associated with the regulation of lifespan in model organisms.[https://www.ncbi.nlm.nih.gov/pubmed/10512855/]
+Thus elevated levels of ketones are conditionary to, and stimulate autophagy. Just as a small group of other metabolic intermediates that affect gene expression via chromatin modifications [https://www.ncbi.nlm.nih.gov/pubmed/22265398/], β-hydroxybutyrate (and butyrate[http://www.jbc.org/content/254/5/1716.long] competitively [https://www.ncbi.nlm.nih.gov/pubmed/18059533/], and at least four major structurally distinct classes[https://www.ncbi.nlm.nih.gov/pubmed/16955068/]) acts as an endogenous inhibitor of HDACs class 1 and 2a.[https://www.ncbi.nlm.nih.gov/pubmed/23223453/], which induces Foxo3a.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/] (Foxo3a is the mammalian ortholog of the stress-responsive transcriptional factor DAF16 that regulates lifespan in worms[https://www.ncbi.nlm.nih.gov/pubmed/20336132/])  Class I HDACs are associated with the regulation of lifespan in model organisms.[https://www.ncbi.nlm.nih.gov/pubmed/10512855/] βOHB delivered via the diet in the form of a synthetic ester improves learning and memory.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619192/]
 Ketogenic diets suppress fatty acid synthesis enzymes [https://www.ncbi.nlm.nih.gov/pubmed/17299079/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781352/] and strongly induce regulation of ketogenic genes, and one of its crucial downstream targets, resulting in increased transcription of ketogenic enzymes [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3119109/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781352/].

← Older revision		Revision as of 13:51, 16 September 2017
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	Thus elevated levels of ketones are conditionary to, and stimulate autophagy. Just as a small group of other metabolic intermediates that affect gene expression via chromatin modifications [https://www.ncbi.nlm.nih.gov/pubmed/22265398/], β-hydroxybutyrate (and butyrate[http://www.jbc.org/content/254/5/1716.long] competitively [https://www.ncbi.nlm.nih.gov/pubmed/18059533/], and at least four major structurally distinct classes[https://www.ncbi.nlm.nih.gov/pubmed/16955068/]) acts as an endogenous inhibitor of HDACs class 1 and 2a.[https://www.ncbi.nlm.nih.gov/pubmed/23223453/], which induces Foxo3a.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/] (Foxo3a is the mammalian ortholog of the stress-responsive transcriptional factor DAF16 that regulates lifespan in worms[https://www.ncbi.nlm.nih.gov/pubmed/20336132/]) Class I HDACs are associated with the regulation of lifespan in model organisms.[https://www.ncbi.nlm.nih.gov/pubmed/10512855/]		Thus elevated levels of ketones are conditionary to, and stimulate autophagy. Just as a small group of other metabolic intermediates that affect gene expression via chromatin modifications [https://www.ncbi.nlm.nih.gov/pubmed/22265398/], β-hydroxybutyrate (and butyrate[http://www.jbc.org/content/254/5/1716.long] competitively [https://www.ncbi.nlm.nih.gov/pubmed/18059533/], and at least four major structurally distinct classes[https://www.ncbi.nlm.nih.gov/pubmed/16955068/]) acts as an endogenous inhibitor of HDACs class 1 and 2a.[https://www.ncbi.nlm.nih.gov/pubmed/23223453/], which induces Foxo3a.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/] (Foxo3a is the mammalian ortholog of the stress-responsive transcriptional factor DAF16 that regulates lifespan in worms[https://www.ncbi.nlm.nih.gov/pubmed/20336132/]) Class I HDACs are associated with the regulation of lifespan in model organisms.[https://www.ncbi.nlm.nih.gov/pubmed/10512855/]
		+
		+	Ketogenic diets suppress fatty acid synthesis enzymes [https://www.ncbi.nlm.nih.gov/pubmed/17299079/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781352/] and strongly induce regulation of ketogenic genes, and one of its crucial downstream targets, resulting in increased transcription of ketogenic enzymes [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3119109/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781352/].
		+	A ketogenic diet also promotes mitochondrial biogenesis [https://www.ncbi.nlm.nih.gov/pubmed/20167576/] and increases expression of SIRT1 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821007/], which is also increased during calorie restriction and regulates a variety of aging-related pathways (reviewed in [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872805/])

	==Antioxidants==		==Antioxidants==

@@ Line 47: / Line 47: @@
 Energy-restricted metabolic states (CR, IF), extend lifespan in animals, not requiring overall reduced caloric intake [https://www.ncbi.nlm.nih.gov/pubmed/23598600/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491655/], but necessarily associated with elevations in ketone bodies. In starvation mode, when liver glycogen is depleted, the major source of fuel for the brains (and other tissues) shifts from glucose to ketone bodies (derived from fatty acids and ketogenic amino acids). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate. Levels of β-hydroxybutyrate increase dramatically on a ketogenic diet [https://www.ncbi.nlm.nih.gov/pubmed/18301085/], after 12–16 hours of fasting [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292859/][https://www.ncbi.nlm.nih.gov/pubmed/6986618/], and after 90 minutes of intense exercise [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1279383/].
-Thus elevated levels of ketones are conditionary to, and stimulate autophagy. Just as a small group of other metabolic intermediates that affect gene expression via chromatin modifications [https://www.ncbi.nlm.nih.gov/pubmed/22265398/], β-hydroxybutyrate (and butyrate[http://www.jbc.org/content/254/5/1716.long], and at least four major structurally distinct classes[https://www.ncbi.nlm.nih.gov/pubmed/16955068/]) acts as an endogenous inhibitor of HDACs class 1 and 2a.[https://www.ncbi.nlm.nih.gov/pubmed/23223453/], which induces Foxo3a.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/] (Foxo3a is the mammalian ortholog of the stress-responsive transcriptional factor DAF16 that regulates lifespan in worms[https://www.ncbi.nlm.nih.gov/pubmed/20336132/])  Class I HDACs are associated with the regulation of lifespan in model organisms.[https://www.ncbi.nlm.nih.gov/pubmed/10512855/]
+Thus elevated levels of ketones are conditionary to, and stimulate autophagy. Just as a small group of other metabolic intermediates that affect gene expression via chromatin modifications [https://www.ncbi.nlm.nih.gov/pubmed/22265398/], β-hydroxybutyrate (and butyrate[http://www.jbc.org/content/254/5/1716.long] competitively [https://www.ncbi.nlm.nih.gov/pubmed/18059533/], and at least four major structurally distinct classes[https://www.ncbi.nlm.nih.gov/pubmed/16955068/]) acts as an endogenous inhibitor of HDACs class 1 and 2a.[https://www.ncbi.nlm.nih.gov/pubmed/23223453/], which induces Foxo3a.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/] (Foxo3a is the mammalian ortholog of the stress-responsive transcriptional factor DAF16 that regulates lifespan in worms[https://www.ncbi.nlm.nih.gov/pubmed/20336132/])  Class I HDACs are associated with the regulation of lifespan in model organisms.[https://www.ncbi.nlm.nih.gov/pubmed/10512855/]
 ==Antioxidants==

@@ Line 45: / Line 45: @@
 ==Ketones==
-Energy-restricted metabolic states (CR, IF), extend lifespan in animals, not require overall reduced caloric intake [https://www.ncbi.nlm.nih.gov/pubmed/23598600/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491655/], but necessarily associated with elevations in ketone bodies. In starvation mode, when liver glycogen is depleted, the major source of fuel for the brains (and other tissues) shifts from glucose to ketone bodies (derived from fatty acids and ketogenic amino acids). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate. Levels of β-hydroxybutyrate increase dramatically on a ketogenic diet [https://www.ncbi.nlm.nih.gov/pubmed/18301085/], after 12–16 hours of fasting [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292859/][https://www.ncbi.nlm.nih.gov/pubmed/6986618/], and after 90 minutes of intense exercise [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1279383/].
+Energy-restricted metabolic states (CR, IF), extend lifespan in animals, not requiring overall reduced caloric intake [https://www.ncbi.nlm.nih.gov/pubmed/23598600/][https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491655/], but necessarily associated with elevations in ketone bodies. In starvation mode, when liver glycogen is depleted, the major source of fuel for the brains (and other tissues) shifts from glucose to ketone bodies (derived from fatty acids and ketogenic amino acids). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate. Levels of β-hydroxybutyrate increase dramatically on a ketogenic diet [https://www.ncbi.nlm.nih.gov/pubmed/18301085/], after 12–16 hours of fasting [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292859/][https://www.ncbi.nlm.nih.gov/pubmed/6986618/], and after 90 minutes of intense exercise [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1279383/].
 Thus elevated levels of ketones are conditionary to, and stimulate autophagy. Just as a small group of other metabolic intermediates that affect gene expression via chromatin modifications [https://www.ncbi.nlm.nih.gov/pubmed/22265398/], β-hydroxybutyrate acts as an endogenous inhibitor of HDACs class 1 and 2a.[https://www.ncbi.nlm.nih.gov/pubmed/23223453/], which induces Foxo3a.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/] (Foxo3a is the mammalian ortholog of the stress-responsive transcriptional factor DAF16 that regulates lifespan in worms[https://www.ncbi.nlm.nih.gov/pubmed/20336132/])  Class I HDACs are associated with the regulation of lifespan in model organisms.[https://www.ncbi.nlm.nih.gov/pubmed/10512855/]