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  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
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We began analyzing https://www.nature.com/articles/nrendo.2017.132, but it redirected us to https://www.nature.com/articles/nrendo.2017.132. The analysis below is for the second page.

Title[redir]:
Targeting thermogenesis in brown fat and muscle to treat obesity and metabolic disease | Nature Reviews Endocrinology
Description:
Targeting thermogenesis in brown fat and skeletal muscle to expend energy and reduce fat mass is a promising therapeutic strategy for treating obesity and related metabolic diseases. Here, Betz and Enerbäck discuss the different molecular pathways regulating thermogenesis in these organs and discuss how they can be therapeutically exploited. Brown fat is emerging as an interesting and promising target for therapeutic intervention in obesity and metabolic disease. Activation of brown fat in humans is associated with marked improvement in metabolic parameters such as levels of free fatty acids and insulin sensitivity. Skeletal muscle is another important organ for thermogenesis, with the capacity to induce energy-consuming futile cycles. In this Review, we focus on how these two major thermogenic organs — brown fat and muscle — act and cooperate to maintain normal body temperature. Moreover, in the light of disease-relevant mechanisms, we explore the molecular pathways that regulate thermogenesis in brown fat and muscle. Brown adipocytes possess a unique cellular mechanism to convert chemical energy into heat: uncoupling protein 1 (UCP1), which can short-circuit the mitochondrial proton gradient. However, recent research demonstrates the existence of several other energy-expending

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Science

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 98,426,998 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We can't figure out the monetization strategy.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Doi.org could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

pubmed, article, google, scholar, cas, brown, tissue, adipose, central, thermogenesis, physiol, nature, fat, humans, adipocytes, cold, obesity, uncoupling, cell, human, mice, white, muscle, ucp, energy, thermogenic, clin, metab, nat, med, protein, endocrinol, biol, content, metabolic, coldinduced, mitochondrial, access, expenditure, mechanisms, adult, plos, gene, van, endocrinology, research, skeletal, temperature, kozak, sci,

Topics {✒️}

nature portfolio journals permissions reprints nature portfolio privacy policy recent research demonstrates swedish research council advertising fatty-acid-dependent ucp1 uncoupling social media regional distribution central efferent pathways skeletal-muscle-based thermogenic mechanisms author information authors east energy-expending 'futile' cycles nature+ nature 448 nature 206 nature 454 nature 387 nature 516 nature case-controlled observational study skeletal-muscle sarcoplasmic reticulum cold-induced brown adipocytes author correspondence tissue-dependent rna expression glucose-intolerant men improves central neural pathways cold-induced adaptive thermogenesis plasmic reticulum ca2+-atpase cold-acclimated rats reevaluated rhythm-generating mechanisms governing synchronized slow-amplitude modulations resist diet-induced obesity van marken lichtenbelt career development grant cold-acclimated ucp1−/− mice de quadrupedibus viviparis central core disease permissions brown adipose tissue springerlink instant access recruits beige adipocytes article betz ucp3 protein content brown fat mitochondria personal data dorsal dermal fate fatty acid synthesis

Questions {❓}

  • Role of UCP homologues in skeletal muscles and brown adipose tissue: mediators of thermogenesis or regulators of lipids as fuel substrate?
  • The 'novel' 'uncoupling' proteins UCP2 and UCP3: what do they really do?

Schema {🗺️}

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         headline:Targeting thermogenesis in brown fat and muscle to treat obesity and metabolic disease
         description: Targeting thermogenesis in brown fat and skeletal muscle to expend energy and reduce fat mass is a promising therapeutic strategy for treating obesity and related metabolic diseases. Here, Betz and Enerbäck discuss the different molecular pathways regulating thermogenesis in these organs and discuss how they can be therapeutically exploited. Brown fat is emerging as an interesting and promising target for therapeutic intervention in obesity and metabolic disease. Activation of brown fat in humans is associated with marked improvement in metabolic parameters such as levels of free fatty acids and insulin sensitivity. Skeletal muscle is another important organ for thermogenesis, with the capacity to induce energy-consuming futile cycles. In this Review, we focus on how these two major thermogenic organs — brown fat and muscle — act and cooperate to maintain normal body temperature. Moreover, in the light of disease-relevant mechanisms, we explore the molecular pathways that regulate thermogenesis in brown fat and muscle. Brown adipocytes possess a unique cellular mechanism to convert chemical energy into heat: uncoupling protein 1 (UCP1), which can short-circuit the mitochondrial proton gradient. However, recent research demonstrates the existence of several other energy-expending 'futile' cycles in both adipocytes and muscle, such as creatine and calcium cycling. These mechanisms can complement or even substitute for UCP1-mediated thermogenesis. Moreover, they expand our view of cold-induced thermogenesis from a special feature of brown adipocytes to a more general physiological principle. Finally, we discuss how thermogenic mechanisms can be exploited to expend energy and hence offer new therapeutic opportunities.
         datePublished:2017-10-23T00:00:00Z
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      headline:Targeting thermogenesis in brown fat and muscle to treat obesity and metabolic disease
      description: Targeting thermogenesis in brown fat and skeletal muscle to expend energy and reduce fat mass is a promising therapeutic strategy for treating obesity and related metabolic diseases. Here, Betz and Enerbäck discuss the different molecular pathways regulating thermogenesis in these organs and discuss how they can be therapeutically exploited. Brown fat is emerging as an interesting and promising target for therapeutic intervention in obesity and metabolic disease. Activation of brown fat in humans is associated with marked improvement in metabolic parameters such as levels of free fatty acids and insulin sensitivity. Skeletal muscle is another important organ for thermogenesis, with the capacity to induce energy-consuming futile cycles. In this Review, we focus on how these two major thermogenic organs — brown fat and muscle — act and cooperate to maintain normal body temperature. Moreover, in the light of disease-relevant mechanisms, we explore the molecular pathways that regulate thermogenesis in brown fat and muscle. Brown adipocytes possess a unique cellular mechanism to convert chemical energy into heat: uncoupling protein 1 (UCP1), which can short-circuit the mitochondrial proton gradient. However, recent research demonstrates the existence of several other energy-expending 'futile' cycles in both adipocytes and muscle, such as creatine and calcium cycling. These mechanisms can complement or even substitute for UCP1-mediated thermogenesis. Moreover, they expand our view of cold-induced thermogenesis from a special feature of brown adipocytes to a more general physiological principle. Finally, we discuss how thermogenic mechanisms can be exploited to expend energy and hence offer new therapeutic opportunities.
      datePublished:2017-10-23T00:00:00Z
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      pageStart:77
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Social Networks {👍}(2)

External Links {🔗}(561)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Foundation
  • Prism.js
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
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Name Servers:

  • josh.ns.cloudflare.com
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CDN Services {📦}

  • Crossref

4.82s.