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Iporuru

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  1. It's quite a high level of exertion. Can you maintain your concentration level on what you're reading? I guess with time and your level of fitness it's not a big deal...
  2. Dean, at what speed (and possibly incline) do you walk on the treadmill?
  3. Proc Nutr Soc. 2020 Apr 15:1-19. doi: 10.1017/S0029665120006928. [Epub ahead of print] Feeding brown fat: dietary phytochemicals targeting non-shivering thermogenesis to control body weight. Horvath C1, Wolfrum C1. Author information Abstract Excessive adipose accumulation, which is the main driver for the development of secondary metabolic complications, has reached epidemic proportions and combined pharmaceutical, educational and nutritional approaches are required to reverse the current rise in global obesity prevalence rates. Brown adipose tissue (BAT) is a unique organ able to dissipate energy and thus a promising target to enhance BMR to counteract a positive energy balance. In addition, active BAT might support body weight maintenance after weight loss to prevent/reduce relapse. Natural products deliver valuable bioactive compounds that have historically helped to alleviate disease symptoms. Interest in recent years has focused on identifying nutritional constituents that are able to induce BAT activity and thereby enhance energy expenditure. This review provides a summary of selected dietary phytochemicals, including isoflavones, catechins, stilbenes, the flavonoids quercetin, luteolin and resveratrol as well as the alkaloids berberine and capsaicin. Most of the discussed phytochemicals act through distinct molecular pathways e.g. sympathetic nerve activation, AMP-kinase signalling, SIRT1 activity or stimulation of oestrogen receptors. Thus, it might be possible to utilise this multitude of pathways to co-activate BAT using a fine-tuned combination of foods or combined nutritional supplements. KEYWORDS: Brown adipose tissue; Browning; Energy expenditure; Phytochemicals; Weight management PMID: 32290888 DOI: 10.1017/S0029665120006928
  4. Another New Zoonotic Virus Disease Emerging In China - Orthohantavirus
  5. Do you know if they ship outside Russia? Could you provide a link to that shop?
  6. Hi Sibiriak Are the masks you bought available online?
  7. We will have to add chronic high-sucrose diet to the list 😉 Chronic high-sucrose diet increases fibroblast growth factor 21 production and energy expenditure in mice Abstract Excess carbohydrate intake causes obesity in humans. On the other hand, acute administration of fructose, glucose or sucrose in experimental animals has been shown to increase the plasma concentration of anti-obesity hormones such as glucagon-like peptide 1 (GLP-1) and Fibroblast growth factor 21 (FGF21), which contribute to reducing body weight. However, the secretion and action of GLP-1 and FGF21 in mice chronically fed a high-sucrose diet has not been investigated. To address the role of anti-obesity hormones in response to increased sucrose intake, we analyzed mice fed a high-sucrose diet, a high-starch diet or a normal diet for 15 weeks. Mice fed a high-sucrose diet showed resistance to body weight gain, in comparison with mice fed a high-starch diet or control diet, due to increased energy expenditure. Plasma FGF21 levels were highest among the three groups in mice fed a high-sucrose diet, whereas no significant difference in GLP-1 levels was observed. Expression levels of uncoupling protein 1 (UCP-1), FGF receptor 1c (FGFR1c) and β-klotho (KLB) mRNA in brown adipose tissue were significantly increased in high sucrose-fed mice, suggesting increases in FGF21 sensitivity and energy expenditure. Expression of carbohydrate responsive element binding protein (ChREBP) mRNA in liver and brown adipose tissue was also increased in high sucrose-fed mice. These results indicate that FGF21 production in liver and brown adipose tissue is increased in high-sucrose diet and participates in resistance to weight gain.
  8. Iporuru

    Do pure amino acids have calories?

    Even worse, they have kilocalories, which makes them unsuitable for human consumption
  9. A new item to be added to the long list of factors associated with increased brown/beige adipose tissue and/or thermogenesis: Dietary alpha‐ketoglutarate promotes beige adipogenesis and prevents obesity in middle‐aged mice Abstract Aging usually involves the progressive development of certain illnesses, including diabetes and obesity. Due to incapacity to form new white adipocytes, adipose expansion in aged mice primarily depends on adipocyte hypertrophy, which induces metabolic dysfunction. On the other hand, brown adipose tissue burns fatty acids, preventing ectopic lipid accumulation and metabolic diseases. However, the capacity of brown/beige adipogenesis declines inevitably during the aging process. Previously, we reported that DNA demethylation in the Prdm16 promoter is required for beige adipogenesis. DNA methylation is mediated by ten–eleven family proteins (TET) using alpha‐ketoglutarate (AKG) as a cofactor. Here, we demonstrated that the circulatory AKG concentration was reduced in middle‐aged mice (10‐month‐old) compared with young mice (2‐month‐old). Through AKG administration replenishing the AKG pool, aged mice were associated with the lower body weight gain and fat mass, and improved glucose tolerance after challenged with high‐fat diet (HFD). These metabolic changes are accompanied by increased expression of brown adipose genes and proteins in inguinal adipose tissue. Cold‐induced brown/beige adipogenesis was impeded in HFD mice, whereas AKG rescued the impairment of beige adipocyte functionality in middle‐aged mice. Besides, AKG administration up‐regulated Prdm16 expression, which was correlated with an increase of DNA demethylation in the Prdm16 promoter. In summary, AKG supplementation promotes beige adipogenesis and alleviates HFD‐induced obesity in middle‐aged mice, which is associated with enhanced DNA demethylation of the Prdm16 gene. ORIGINAL ARTICLE Open Access Qiyu Tian, Junxing Zhao, Qiyuan Yang, Bo Wang, Jeanene M. Deavila, Mei-Jun Zhu, Min Du First published: 06 November 2019 https://doi.org/10.1111/acel.13059 And an earlier paper: Cell Metab. 2016 Oct 11;24(4):542-554. doi: 10.1016/j.cmet.2016.08.010. Epub 2016 Sep 15. AMPK/α-Ketoglutarate Axis Dynamically Mediates DNA Demethylation in the Prdm16 Promoter and Brown Adipogenesis. Yang Q1, Liang X1, Sun X2, Zhang L3, Fu X1, Rogers CJ1, Berim A4, Zhang S2, Wang S1, Wang B1, Foretz M5, Viollet B5, Gang DR4, Rodgers BD1, Zhu MJ2, Du M6. Author information 1 Washington Center for Muscle Biology and Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA. 2 School of Food Sciences, Washington State University, Pullman, WA 99164, USA. 3 Washington Center for Muscle Biology and Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA; Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, China. 4 Institute of Biological Chemistry, Washington State University, Pullman, WA 99164, USA. 5 INSERM U1016, Institut Cochin, 75014 Paris, France; CNRS UMR 8104, 75014 Paris, France; Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France. 6 Washington Center for Muscle Biology and Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA; Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, Beijing 100194, China. Electronic address: min.du@wsu.edu. Abstract Promoting brown adipose tissue (BAT) development is an attractive strategy for the treatment of obesity, as activated BAT dissipates energy through thermogenesis; however, the mechanisms controlling BAT formation are not fully understood. We hypothesized that as a master regulator of energy metabolism, AMP-activated protein kinase (AMPK) may play a direct role in the process and found that AMPKα1 (PRKAA1) ablation reduced Prdm16 expression and impaired BAT development. During early brown adipogenesis, the cellular levels of α-ketoglutarate (αKG), a key metabolite required for TET-mediated DNA demethylation, were profoundly increased and required for active DNA demethylation of the Prdm16 promoter. AMPKα1 ablation reduced isocitrate dehydrogenase 2 activity and cellular αKG levels. Remarkably, postnatal AMPK activation with AICAR or metformin rescued obesity-induced suppression of brown adipogenesis and thermogenesis. In summary, AMPK is essential for the epigenetic control of BAT development through αKG, thus linking a metabolite to progenitor cell differentiation and thermogenesis. Copyright © 2016 Elsevier Inc. All rights reserved. KEYWORDS: DNA demethylation; Prkaa1; brown adipogenesis PMID: 27641099 PMCID: PMC5061633 DOI: 10.1016/j.cmet.2016.08.010 [Indexed for MEDLINE] Free PMC Article
  10. A new study: https://www.ncbi.nlm.nih.gov/pubmed/31694884 Proc Natl Acad Sci U S A. 2019 Nov 6. pii: 201909917. doi: 10.1073/pnas.1909917116. [Epub ahead of print] Adipose tissue NAD+ biosynthesis is required for regulating adaptive thermogenesis and whole-body energy homeostasis in mice. Yamaguchi S1, Franczyk MP1, Chondronikola M1, Qi N2, Gunawardana SC3, Stromsdorfer KL1, Porter LC1, Wozniak DF4,5, Sasaki Y6, Rensing N7, Wong M7, Piston DW3, Klein S1,3, Yoshino J8,9. Author information 1 Center for Human Nutrition, Washington University School of Medicine, St. Louis, MO 63110. 2 Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109. 3 Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110. 4 Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110. 5 Taylor Family Institute for Innovative Psychiatric Research, Washington University School of Medicine, St. Louis, MO 63110. 6 Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110. 7 Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110. 8 Center for Human Nutrition, Washington University School of Medicine, St. Louis, MO 63110; jyoshino@wustl.edu. 9 Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110. Abstract Nicotinamide adenine dinucleotide (NAD+) is a critical coenzyme for cellular energy metabolism. The aim of the present study was to determine the importance of brown and white adipose tissue (BAT and WAT) NAD+ metabolism in regulating whole-body thermogenesis and energy metabolism. Accordingly, we generated and analyzed adipocyte-specific nicotinamide phosphoribosyltransferase (Nampt) knockout (ANKO) and brown adipocyte-specific Nampt knockout (BANKO) mice because NAMPT is the rate-limiting NAD+ biosynthetic enzyme. We found ANKO mice, which lack NAMPT in both BAT and WAT, had impaired gene programs involved in thermogenesis and mitochondrial function in BAT and a blunted thermogenic (rectal temperature, BAT temperature, and whole-body oxygen consumption) response to acute cold exposure, prolonged fasting, and administration of β-adrenergic agonists (norepinephrine and CL-316243). In addition, the absence of NAMPT in WAT markedly reduced adrenergic-mediated lipolytic activity, likely through inactivation of the NAD+-SIRT1-caveolin-1 axis, which limits an important fuel source fatty acid for BAT thermogenesis. These metabolic abnormalities were rescued by treatment with nicotinamide mononucleotide (NMN), which bypasses the block in NAD+ synthesis induced by NAMPT deficiency. Although BANKO mice, which lack NAMPT in BAT only, had BAT cellular alterations similar to the ANKO mice, BANKO mice had normal thermogenic and lipolytic responses. We also found NAMPT expression in supraclavicular adipose tissue (where human BAT is localized) obtained from human subjects increased during cold exposure, suggesting our finding in rodents could apply to people. These results demonstrate that adipose NAMPT-mediated NAD+ biosynthesis is essential for regulating adaptive thermogenesis, lipolysis, and whole-body energy metabolism. KEYWORDS: NAD; adipose tissue; energy metabolism; lipolysis; thermogenesis PMID: 31694884 DOI: 10.1073/pnas.1909917116
  11. Iporuru

    Could a person weigh less on a ketogenic diet?

    From Wikipedia: "Treatment of anorexia involves restoring a healthy weight, treating the underlying psychological problems, and addressing behaviors that promote the problem." (https://en.wikipedia.org/wiki/Anorexia_nervosa#Treatment) I believe a fed anorexic troll will still be a troll so treating the underlying psychological problems would probably be most effective, as others have also pointed out
  12. Iporuru

    Could a person weigh less on a ketogenic diet?

    Don't feed the troll (pun intended) 😉
  13. Health in old age is a lifelong affair Reduced food intake in old mice can no longer improve health https://www.mpg.de/14021239/1017-balt-110438-health-in-old-age-is-a-lifelong-affair
  14. I have come across this study (DOI: 10.1038/35046114) which says: https://www.researchgate.net/publication/12210344_Coenzyme_Q_is_an_obligatory_cofactor_for_uncoupling_protein_function Coenzyme Q is an obligatory cofactor for uncoupling protein function "Uncoupling proteins (UCPs) are thought to be intricately controlled uncouplers that are responsible for the futile dissipation of mitochondrial chemiosmotic gradients, producing heat rather than ATP. They occur in many animal and plant cells and form a subfamily of the mitochondrial carrier family. Physiological uncoupling of oxidative phosphorylation must be strongly regulated to avoid deterioration of the energy supply and cell death, which is caused by toxic uncouplers. However, an H+ transporting uncoupling function is well established only for UCP1 from brown adipose tissue, and the regulation of UCP1 by fatty acids, nucleotides and pH remains controversial. The failure of UCP1 expressed in Escherichia coli inclusion bodies to carry out fatty-acid-dependent H+ transport activity inclusion bodies made us seek a native UCP cofactor. Here we report the identification of coenzyme Q (ubiquinone) as such a cofactor. On addition of CoQ10 to reconstituted UCP1 from inclusion bodies, fatty-acid-dependent H+ transport reached the same rate as with native UCP1. The H+ transport was highly sensitive to purine nucleotides, and activated only by oxidized but not reduced CoQ. H+ transport of native UCP1 correlated with the endogenous CoQ content" and another study (PMID: 28811612) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5557856/ Coenzyme Q10 Improves Lipid Metabolism and Ameliorates Obesity by Regulating CaMKII-Mediated PDE4 Inhibition "BAT thermogenesis induces expression of uncoupling protein 1 (Ucp1) and other genes, promoting lipolysis, mitochondrial biogenesis, and β-oxidation of fatty acids. Our experiment showed that mRNA expression of Ucp1 and other thermogenesis-related genes was significantly increased in BAT from KKAy mice supplemented with CoQ10H2 compared with the control group, suggesting that the CoQ10H2 group had increased BAT thermogenic activity (Fig. 2C). " I don't think they have been mentioned before
  15. Iporuru

    Olive oil? Healthy or not?!

    See also what Dean wrote about this overview:
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