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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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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
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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
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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:
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pageEnd:211
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Metabolic efficiency
obesity
ob/ob mice
db/db mice
non-shivering thermogenesis
cold adaptation
Internal Medicine
Metabolic Diseases
Human Physiology
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