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Danes je Če nov 23, 2017 21:29

Keto/Low carb študije

Moderatorji: UrosS, Metka, Stasa, Grom

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Grom

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Šefe

Vnosov: 60527

Pridružen: Če sep 23, 2004 18:35

Odgovor Sr okt 18, 2017 15:40

Re: Keto/Low carb študije

A ketogenic diet supplemented with medium-chain triglycerides enhances the anti-tumor and anti-angiogenic efficacy of chemotherapy on neuroblastoma xenografts in a CD1-nu mouse model

Neuroblastoma (NB) is a pediatric malignancy characterized by a marked reduction in aerobic energy metabolism. Recent preclinical data indicate that targeting this metabolic phenotype by a ketogenic diet (KD), especially in combination with calorie restriction, slows tumor growth and enhances metronomic cyclophosphamide (CP) therapy of NB xenografts. Because calorie restriction would be contraindicated in most cancer patients, the aim of the present study was to optimize the KD such that the tumors are sensitized to CP without the need of calorie restriction. In a NB xenograft model, metronomic CP was combined with KDs of different triglyceride compositions and fed to CD1-nu mice ad libitum. Metronomic CP in combination with a KD containing 8-carbon medium-chain triglycerides exerted a robust anti-tumor effect, suppressing growth and causing a significant reduction of tumor blood-vessel density and intratumoral hemorrhage, accompanied by activation of AMP-activated protein kinase in NB cells. Furthermore, the KDs caused a significant reduction in the serum levels of essential amino acids, but increased those of serine, glutamine and glycine. Our data suggest that targeting energy metabolism by a modified KD may be considered as part of a multimodal treatment regimen to improve the efficacy of classic anti-NB therapy.
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Grom

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Šefe

Vnosov: 60527

Pridružen: Če sep 23, 2004 18:35

Odgovor Sr okt 18, 2017 15:41

Re: Keto/Low carb študije

Ketogenic metabolism inhibits histone deacetylase (HDAC) and reduces oxidative stress after spinal cord injury in rat

Ketogenic metabolism inhibited HDAC activity and increased histone acetylation in spinal cord tissue in rats.
Ketogenic metabolism increased the expression of oxidative stress resistance gene Foxo3a and Mt2 in rat spinal cord.
The changes in histone acetylation and gene expression caused by Ketogenic metabolism may contribute to oxidative stress resistance after acute SCI.
The anti-oxidative stress capacity of three ketogenic metabolism groups seemed to be βOHB dose-dependent.

Abstract

The aim of this study is to investigate the effect of ketogenic metabolism, induced by different diet interventions, on histone acetylation and its potential antioxidant capacity to injured spinal cord tissue in rats. 72 male Sprague–Dawley rats were randomly divided into 4 groups, fed with ketogenic diet (KD), every other day fasting (EODF), every other day ketogenic diet (EODKD) and standard diet (SD) respectively for 2 weeks. β-Hydroxybutyrate (βOHB) concentration was measured both in serum and cerebrospinal fluid (CSF). C5 spinal cord tissue was harvested before, at 3 h and 24 h after injury for analysis of HDAC activity, histone acetylation and oxidative makers. All three dietary interventions resulted in a significant increase of βOHB level in both serum and CSF, and inhibited HDAC activity by 31–43% in spinal cord. Moreover, the expressions of acetylated histone AcH3K9 and AcH3K14 were significantly increased. Anti-oxidative stress genes Foxo3a and Mt2 and related proteins, such as Mitochondrial superoxide dismutase (SOD), FOXO3a, catalase were increased in dietary intervention groups. After SCI, high ketogenic metabolism demonstrated significant reduction of the expression of lipid peroxidation factors malondialdehyde (MDA), and this might contribute to the reported neuroprotection of the spinal cord from oxidative damage possibly mediated by increasing SOD. The result of this study suggested that by inhibiting HDAC activity and modifying related gene transcription, ketogenic metabolism, induced by KD, EODF or EODKD, might reduce oxidative damage in spinal cord tissue after acute injury.
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Grom

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Šefe

Vnosov: 60527

Pridružen: Če sep 23, 2004 18:35

Odgovor Sr okt 18, 2017 15:43

Re: Keto/Low carb študije

Ketone Body Acetoacetate Buffers Methylglyoxal via a Non-enzymatic Conversion during Diabetic and Dietary Ketosis

In vivo reaction between MG and AcAcO yields the novel metabolite 3-HHD
The rate of reaction matches that of known pharmacological scavengers of MG
A metabolite-alkyne-tagging strategy clarifies the reductive metabolism of 3-HHD
MG-scavenging expands the known biological functions of ketone bodies

Summary

The α-oxoaldehyde methylglyoxal is a ubiquitous and highly reactive metabolite known to be involved in aging- and diabetes-related diseases. If not detoxified by the endogenous glyoxalase system, it exerts its detrimental effects primarily by reacting with biopolymers such as DNA and proteins. We now demonstrate that during ketosis, another metabolic route is operative via direct non-enzymatic aldol reaction between methylglyoxal and the ketone body acetoacetate, leading to 3-hydroxyhexane-2,5-dione. This novel metabolite is present at a concentration of 10%–20% of the methylglyoxal level in the blood of insulin-starved patients. By employing a metabolite-alkyne-tagging strategy it is clarified that 3-hydroxyhexane-2,5-dione is further metabolized to non-glycating species in human blood. The discovery represents a new direction within non-enzymatic metabolism and within the use of alkyne-tagging for metabolism studies and it revitalizes acetoacetate as a competent endogenous carbon nucleophile.
Introduction

The elucidation of the major pathways of intermediary metabolism during the 1930s and 1940s constitutes one of the golden eras of twentieth-century biochemical research. Convergence toward the now canonical catabolic and anabolic processes, such as glycolysis, the tricarboxylic acid cycle and the β-oxidation pathways was, however, side-tracked in several instances by alternative hypotheses. One of the more spectacular involved a putative link between the metabolism of fatty acids and carbohydrates, reported in the 1930s by Henze and co-workers. This hypothesis arose from the observation that a product of fatty acid catabolism, acetoacetate (AcAcO), under preparative conditions undergoes a chemical reaction with the 3-carbon α-oxoaldehyde methylglyoxal (MG) (Henze, 1930, Henze and Müller, 1930). The latter was at the time speculated as being a pivotal intermediate of glycolysis (Neuberg and Kerb, 1914). The product of this reaction, 3-hydroxyhexane-2,5-dione (3-HHD 1) (Figure 1), appeared to be labile toward chemical oxidations, eventually breaking down to pyruvate (Henze, 1930) and thus providing an exciting metabolic possibility for converting fatty acids into carbohydrates (Stöhr and Henze, 1932). However, the subsequent discovery of the phosphorylated intermediates of glycolysis (Embden et al., 1933) put an end to the so-called “methylglyoxal hypothesis” and the hypothetical 3-HHD-forming reaction was forgotten. MG, in fact, is a glycolytic side product generated by spontaneous elimination of phosphate from triosephosphates and through non-enzymatic conversion of sugars, amino acids, and even ketone bodies (Maessen et al., 2015, Matafome et al., 2013, Milligan and Baldwin, 1967, Thornalley, 1996). Despite the evolution of efficient enzymatic detoxification systems (glyoxalase I and II) that are ubiquitous throughout the kingdoms of life (Thornalley, 1996), and despite the very low endogenous levels of MG, e.g., in plasma (140 nM [normal] to 340 nM [diabetic ketosis]) (Lu et al., 2011), MG is a source of biological damage through its ability to chemically modify proteinogenic lysine and arginine residues as well as nucleic acids resulting in a series of advanced glycation end products (AGEs) (Thornalley, 1996). MG and associated AGEs are linked to several aging-related pathologies (Maessen et al., 2015) and elevated levels of MG present in diabetic patients mediate various complications associated with this disease (Bierhaus et al., 2012, Brownlee, 2005, McLellan et al., 1994, Thornalley, 1996). Our understanding of the biology of non-enzymatic post-translational modifications (PTMs) is likely quite rudimentary, notwithstanding the high importance of such processes as demonstrated by a number of recent studies (Baeza et al., 2015, Moellering and Cravatt, 2013, Wang et al., 2014). For instance, the discovery of a non-enzymatic regulatory mechanism within the glycolytic pathway (Moellering and Cravatt, 2013) is a finding that demonstrates that even the most extensively studied cellular pathways may hold additional complexity. In comparison with non-enzymatic PTMs, the non-enzymatic metabolome is an even less-explored frontier of biology (Keller et al., 2015). Although 3-HHD initially turned out being a metabolic mirage, the co-occurrence of elevated concentrations of both MG and AcAcO during diabetic ketosis (Lu et al., 2011) suggested to us that 3-HHD might indeed be formed under such pathophysiological conditions.

In this article we provide the first evidence for the presence of 3-HHD in the blood of ketotic individuals, and demonstrate that the reaction of AcAcO with MG kinetically can compete with known pharmacological scavengers of MG. Furthermore, using a novel metabolite-tagging strategy, we show that 3-HHD primarily undergoes reductive metabolism to non-glycating species in human blood, although 3-HHD is also capable of modifying proteins.
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Grom

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Šefe

Vnosov: 60527

Pridružen: Če sep 23, 2004 18:35

Odgovor Sr okt 18, 2017 15:45

Re: Keto/Low carb študije

Ketogenic Diet Reduces Midlife Mortality and Improves Memory in Aging Mice


Feeding isoprotein ketogenic diet to mice every other week (Cyclic KD) avoids obesity
Cyclic KD reduces midlife mortality with no change in maximum lifespan
Cyclic KD prevents memory decline with modest other healthspan effects
Gene expression of KD is similar to high-fat diet, except for activation of PPARα targets

Summary

Ketogenic diets recapitulate certain metabolic aspects of dietary restriction such as reliance on fatty acid metabolism and production of ketone bodies. We investigated whether an isoprotein ketogenic diet (KD) might, like dietary restriction, affect longevity and healthspan in C57BL/6 male mice. We find that Cyclic KD, KD alternated weekly with the Control diet to prevent obesity, reduces midlife mortality but does not affect maximum lifespan. A non-ketogenic high-fat diet (HF) fed similarly may have an intermediate effect on mortality. Cyclic KD improves memory performance in old age, while modestly improving composite healthspan measures. Gene expression analysis identifies downregulation of insulin, protein synthesis, and fatty acid synthesis pathways as mechanisms common to KD and HF. However, upregulation of PPARα target genes is unique to KD, consistent across tissues, and preserved in old age. In all, we show that a non-obesogenic ketogenic diet improves survival, memory, and healthspan in aging mice.
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Grom

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Šefe

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Pridružen: Če sep 23, 2004 18:35

Odgovor Po nov 06, 2017 18:14

Re: Keto/Low carb študije

Keto-adaptation enhances exercise performance and body composition responses to training in endurance athletes
Fionn T. McSwiney
, Bruce Wardrop
, Parker N. Hyde
, Richard A. Lafountain
, Jeff S. Volek


Abstract
Background

Low-carbohydrate diets have recently grown in popularity among endurance athletes, yet little is known about the long-term (>4 wk) performance implications of consuming a low-carbohydrate high fat ketogenic diet (LCKD) in well-trained athletes.
Methods

Twenty male endurance-trained athletes (age 33 ± 11y, body mass 80 ± 11kg; BMI 24.7 ± 3.1 kg/m2) who habitually consumed a carbohydrate-based diet, self-selected into a high-carbohydrate (HC) group (n = 11, %carbohydrate:protein:fat = 65:14:20), or a LCKD group (n = 9, 6:17:77). Both groups performed the same training intervention (endurance, strength and high intensity interval training (HIIT)). Prior to and following successful completion of 12-weeks of diet and training, participants had their body composition assessed, and completed a 100km time trial (TT), six second (SS) sprint, and a critical power test (CPT). During post-intervention testing the HC group consumed 30–60g/h carbohydrate, whereas the LCKD group consumed water, and electrolytes.
Results

The LCKD group experienced a significantly greater decrease in body mass (HC -0.8 kg, LCKD -5.9 kg; P = 0.009, effect size (ES): 0.338) and percentage body fat percentage (HC -0.7%, LCKD -5.2%; P = 0.008, ES: 0.346). Fasting serum beta-hydroxybutyrate (βHB) significantly increased from 0.1 at baseline to 0.5 mmol/L in the LCKD group (P = 0.011, ES: 0.403) in week 12. There was no significant change in performance of the 100 km TT between groups (HC -1.13 min.sec, LCKD -4.07 min.sec, P = 0.057, ES: 0.196). SS sprint peak power increased by 0.8 watts per kilogram bodyweight (w/kg) in the LCKD group, versus a -0.1 w/kg reduction in the HC group (P = 0.025, ES: 0.263). CPT peak power decreased by -0.7w/kg in the HC group, and increased by 1.4 w/kg in the LCKD group (P = 0.047, ES: 0.212). Fat oxidation in the LCKD group was significantly greater throughout the 100km TT.
Conclusions

Compared to a HC comparison group, a 12-week period of keto-adaptation and exercise training, enhanced body composition, fat oxidation during exercise, and specific measures of performance relevant to competitive endurance athletes.
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Grom

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Šefe

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Pridružen: Če sep 23, 2004 18:35

Odgovor Po nov 06, 2017 18:32

Re: Keto/Low carb študije

A Ketone Ester Drink Lowers Human Ghrelin and Appetite


Author contributions: BJS, KC, and PJC designed the research studies. BJS, PJC, HdW and RDE carried out the studies. BJS, HdW, and MC analyzed the data. BJS wrote the paper with help from MC, HdW, and KC. HdW had primary responsibility for the final content. All authors read and approved the final manuscript.

Clinical trial registration: Research Ethics Committee (NHS Queen's Square 14/LO/0288), www.hra.nhs.uk.

Abstract
Objective

The ketones d-β-hydroxybutyrate (BHB) and acetoacetate are elevated during prolonged fasting or during a “ketogenic” diet. Although weight loss on a ketogenic diet may be associated with decreased appetite and altered gut hormone levels, it is unknown whether such changes are caused by elevated blood ketones. This study investigated the effects of an exogenous ketone ester (KE) on appetite.
Methods

Following an overnight fast, subjects with normal weight (n = 15) consumed 1.9 kcal/kg of KE, or isocaloric dextrose (DEXT), in drinks matched for volume, taste, tonicity, and color. Blood samples were analyzed for BHB, glucose, insulin, ghrelin, glucagon-like peptide 1 (GLP-1), and peptide tyrosine tyrosine (PYY), and a three-measure visual analogue scale was used to measure hunger, fullness, and desire to eat.
Results

KE consumption increased blood BHB levels from 0.2 to 3.3 mM after 60 minutes. DEXT consumption increased plasma glucose levels between 30 and 60 minutes. Postprandial plasma insulin, ghrelin, GLP-1, and PYY levels were significantly lower 2 to 4 hours after KE consumption, compared with DEXT consumption. Temporally related to the observed suppression of ghrelin, reported hunger and desire to eat were also significantly suppressed 1.5 hours after consumption of KE, compared with consumption of DEXT.
Conclusions

Increased blood ketone levels may directly suppress appetite, as KE drinks lowered plasma ghrelin levels, perceived hunger, and desire to eat.
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Grom

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Šefe

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Pridružen: Če sep 23, 2004 18:35

Odgovor Po nov 13, 2017 22:00

Re: Keto/Low carb študije

Epigenetic mechanisms underlying lifespan and age-related effects of dietary restriction and the ketogenic diet.
Moreno CL1, Mobbs CV2.
Author information
Abstract

Aging constitutes the central risk factor for major diseases including many forms of cancer, neurodegeneration, and cardiovascular diseases. The aging process is characterized by both global and tissue-specific changes in gene expression across taxonomically diverse species. While aging has historically been thought to entail cell-autonomous, even stochastic changes, recent evidence suggests that modulation of this process can be hierarchal, wherein manipulations of nutrient-sensing neurons (e.g., in the hypothalamus) produce peripheral effects that may modulate the aging process itself. The most robust intervention extending lifespan, plausibly impinging on the aging process, involves different modalities of dietary restriction (DR). Lifespan extension by DR is associated with broad protection against diseases (natural and engineered). Here we review potential epigenetic processes that may link lifespan to age-related diseases, particularly in the context of DR and (other) ketogenic diets, focusing on brain and hypothalamic mechanisms.
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Grom

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Šefe

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Pridružen: Če sep 23, 2004 18:35

Odgovor To nov 14, 2017 15:40

Re: Keto/Low carb študije

10 patients, 10 years – long term follow-up of cardiovascular risk factors in Glut1 Deficiency treated with ketogenic diet therapies: a prospective, multicenter case series

Highlights

•Long-term follow-up on cardiovascular risk of ketogenic diets refutes prior reports.
•To evaluate cardiovascular risks an at least 5 year follow-up is mandatory.
•Initial dyslipidaemia resolves over time and remains normal at 10 years.
•Carotid intima-media thickness does not increase during long-term application.
•Ketogenic diets are still the treatment of choice for Glut1 Deficiency.

Abstract
Background and Aims

Glut1 Deficiency (Glut1D) is caused by impaired glucose transport into brain. The resulting epileptic encephalopathy and movement disorders can be treated effectively by high-fat carbohydrate-restricted ketogenic diets (KDT) mimicking fasting and providing ketones as an alternative cerebral fuel. Recently 6-24 months follow-ups of epileptic patients reported elevated blood lipids and intima thickening of the carotid artery raising concerns about potential cardiovascular risks by KDTs. To further clarify potential cardiovascular risks on ketogenic diets therapy.
Methods

Between August 2001 and January 2008 we enrolled Glut1D patients on KDT at two hospitals in Germany in this prospective, multicenter case series. The minimal follow up was 10 years. Standard deviation scores (SDS) of body mass index (BMI), total cholesterol (TC), HDL-/LDL cholesterol and triglycerides (TG) before initiation of KDT were compared with the respective values at 6 months, 2, 5 years and 10 years after initiation. After 10 years on KDT cardiovascular risk, assessed by BMI, carotid intima-media thickness (CIMT) measurement and blood pressure, was compared to a healthy reference population (n=550).
Results

Baseline and 10 year follow-up investigations were available from 10 individuals with Glut1D on KDT. After two years on KDT BMI increased significantly, while total cholesterol, HDL-cholesterol, and LDL-cholesterol decreased. Within 3-5 years on KDT these differences disappeared, and after 10 years blood lipid parameters reflected the situation at initiation of KDT. Before initiation of KDT one child had dyslipidaemia, but no child after 10 years. No significant differences were observed with respect to BMI SDS (p=0.26), CIMT (p=0.63) or systolic and diastolic blood pressure SDS (p=0.11 and p=0.37, respectively) in Glut1D children treated with KDT for ≥ 10 years compared to healthy controls.
Conclusions

In contrast to previous short-term reports on adverse effects of KDTs, 10-year follow-up did not identify cardiovascular risks of dietary treatment for Glut1D.
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Grom

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Šefe

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Pridružen: Če sep 23, 2004 18:35

Odgovor To nov 14, 2017 16:08

Re: Keto/Low carb študije

Ketone body 3-hydroxybutyrate mimics calorie restriction via the Nrf2 activator, fumarate, in the retina


Summary

Calorie restriction (CR) being the most robust dietary intervention provides various health benefits. D-3-hydroxybutyrate (3HB), a major physiological ketone, has been proposed as an important endogenous molecule for CR. To investigate the role of 3HB in CR, we investigated potential shared mechanisms underlying increased retinal 3HB induced by CR and exogenously applied 3HB without CR to protect against ischemic retinal degeneration. The repeated elevation of retinal 3HB, with or without CR, suppressed retinal degeneration. Metabolomic analysis showed that the antioxidant pentose phosphate pathway and its limiting enzyme, glucose-6-phosphate dehydrogenase (G6PD), were concomitantly preserved. Importantly, the upregulation of nuclear factor erythroid 2 p45-related factor 2 (Nrf2), a regulator of G6PD, and elevation of the tricarboxylic acid cycle's Nrf2 activator, fumarate, were also shared. Together, our findings suggest that CR provides retinal antioxidative defense by 3HB through the antioxidant Nrf2 pathway via modification of a tricarboxylic acid cycle intermediate during 3HB metabolism.
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