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We began analyzing https://link.springer.com/article/10.1007/BF00283754, but it redirected us to https://link.springer.com/article/10.1007/BF00283754. The analysis below is for the second page.

Title[redir]:
Thermogenesis in diabetes-obesity syndromes in mutant mice | Diabetologia
Description:
The two mouse mutants, obese (ob) and diabetes (db), cause similar diabetes-obesity syndromes that are characterized by a marked increase in apparent metabolic efficiency with regard to utilization of energy. A failure to thermoregulate in a normal fashion would save energy which could then be diverted to other functions and be reflected as increased metabolic efficiency. This study assesses the contribution of a defect in thermogenesis to the increased metabolic efficiency. Thermogenesis in obese (ob) and diabetes (db) mutant mice was quantified at various environmental temperatures. Both mutants maintained body temperatures near normal when maintained at ambient temperatures (23 °C), and if exposed to cold at 10 °C for a brief period, became cold-adapted and would survive indefinitely at 4°C. Rectal temperatures of mutants maintained at 4 °C were only 1 °–2 °C less than those seen in normal mice. This maintenance of nearly normal body temperature at temperatures less than thermoneutral was reflected by increased food consumption in all mice maintained in the cold. The data presented suggest that the defect in thermogenesis in both mutants is not a major cause of the increased metabolic efficiency. Hyperinsulinaemia, a consistent feature of both mutants, might by increasing anabolic processes (synthesis) and decreasing degradation spare energy normally used for tissue turnover and account for some of this increased metabolic efficiency.

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  • Education
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Keywords {🔍}

google, scholar, mice, thermogenesis, obese, article, metabolic, energy, tissue, cold, adipose, diabetes, efficiency, temperatures, trayhurn, obob, brown, privacy, cookies, diabetologia, syndromes, coleman, mouse, mutants, increased, physiol, obesity, lean, nonshivering, content, data, publish, research, search, diabetesobesity, mutant, download, normal, maintained, genetically, nature, information, journal, defect, body, thermoregulatory, discover, metabolism, development, pairfed,

Topics {✒️}

similar diabetes-obesity syndromes long-term thermoregulatory adaptations apparent metabolic efficiency increased metabolic efficiency obese ob/ob mice diabetes-obesity syndromes inherited diabetes syndromes privacy choices/manage cookies high fat brown adipose tissue related subjects main content log reduced energy expenditure mice pair-fed genetically diabetes-obese hereditary obese mice european economic area increasing anabolic processes transcriptomic network underlying vander tuig jc free fatty acids maintenance energy requirements diet-induced thermogenesis data presented suggest conditions privacy policy blood sugar determinations normal body temperature increased food consumption db/db high-carbohydrate diet lean mice fed regional blood flow accepting optional cookies article coleman scope submit manuscript +-atpase enzyme units search search journal finder publish biological research coleman rights ob/ob jackson laboratory mutant mice article cite himms-hagen rothwell nj save energy energy balance energy retention personal data

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Thermogenesis in diabetes-obesity syndromes in mutant mice
         description:The two mouse mutants, obese (ob) and diabetes (db), cause similar diabetes-obesity syndromes that are characterized by a marked increase in apparent metabolic efficiency with regard to utilization of energy. A failure to thermoregulate in a normal fashion would save energy which could then be diverted to other functions and be reflected as increased metabolic efficiency. This study assesses the contribution of a defect in thermogenesis to the increased metabolic efficiency. Thermogenesis in obese (ob) and diabetes (db) mutant mice was quantified at various environmental temperatures. Both mutants maintained body temperatures near normal when maintained at ambient temperatures (23 °C), and if exposed to cold at 10 °C for a brief period, became cold-adapted and would survive indefinitely at 4°C. Rectal temperatures of mutants maintained at 4 °C were only 1 °–2 °C less than those seen in normal mice. This maintenance of nearly normal body temperature at temperatures less than thermoneutral was reflected by increased food consumption in all mice maintained in the cold. The data presented suggest that the defect in thermogenesis in both mutants is not a major cause of the increased metabolic efficiency. Hyperinsulinaemia, a consistent feature of both mutants, might by increasing anabolic processes (synthesis) and decreasing degradation spare energy normally used for tissue turnover and account for some of this increased metabolic efficiency.
         datePublished:
         dateModified:
         pageStart:205
         pageEnd:211
         sameAs:https://doi.org/10.1007/BF00283754
         keywords:
            Metabolic efficiency
            obesity
             ob/ob mice
             db/db mice
            non-shivering thermogenesis
            cold adaptation
            Internal Medicine
            Metabolic Diseases
            Human Physiology
         image:
         isPartOf:
            name:Diabetologia
            issn:
               1432-0428
               0012-186X
            volumeNumber:22
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer-Verlag
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:D. L. Coleman
               affiliation:
                     name:The Jackson Laboratory
                     address:
                        name:The Jackson Laboratory, Bar Harbor, USA
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Thermogenesis in diabetes-obesity syndromes in mutant mice
      description:The two mouse mutants, obese (ob) and diabetes (db), cause similar diabetes-obesity syndromes that are characterized by a marked increase in apparent metabolic efficiency with regard to utilization of energy. A failure to thermoregulate in a normal fashion would save energy which could then be diverted to other functions and be reflected as increased metabolic efficiency. This study assesses the contribution of a defect in thermogenesis to the increased metabolic efficiency. Thermogenesis in obese (ob) and diabetes (db) mutant mice was quantified at various environmental temperatures. Both mutants maintained body temperatures near normal when maintained at ambient temperatures (23 °C), and if exposed to cold at 10 °C for a brief period, became cold-adapted and would survive indefinitely at 4°C. Rectal temperatures of mutants maintained at 4 °C were only 1 °–2 °C less than those seen in normal mice. This maintenance of nearly normal body temperature at temperatures less than thermoneutral was reflected by increased food consumption in all mice maintained in the cold. The data presented suggest that the defect in thermogenesis in both mutants is not a major cause of the increased metabolic efficiency. Hyperinsulinaemia, a consistent feature of both mutants, might by increasing anabolic processes (synthesis) and decreasing degradation spare energy normally used for tissue turnover and account for some of this increased metabolic efficiency.
      datePublished:
      dateModified:
      pageStart:205
      pageEnd:211
      sameAs:https://doi.org/10.1007/BF00283754
      keywords:
         Metabolic efficiency
         obesity
          ob/ob mice
          db/db mice
         non-shivering thermogenesis
         cold adaptation
         Internal Medicine
         Metabolic Diseases
         Human Physiology
      image:
      isPartOf:
         name:Diabetologia
         issn:
            1432-0428
            0012-186X
         volumeNumber:22
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer-Verlag
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:D. L. Coleman
            affiliation:
                  name:The Jackson Laboratory
                  address:
                     name:The Jackson Laboratory, Bar Harbor, USA
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Diabetologia
      issn:
         1432-0428
         0012-186X
      volumeNumber:22
Organization:
      name:Springer-Verlag
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:The Jackson Laboratory
      address:
         name:The Jackson Laboratory, Bar Harbor, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:D. L. Coleman
      affiliation:
            name:The Jackson Laboratory
            address:
               name:The Jackson Laboratory, Bar Harbor, USA
               type:PostalAddress
            type:Organization
PostalAddress:
      name:The Jackson Laboratory, Bar Harbor, USA

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