Diabetologie und Stoffwechsel 2017; 12(S 01): S1-S84
DOI: 10.1055/s-0037-1601731
Poster: *Poster + Kurzpräsentation
Typ-2-Diabetes II – Pathophysiologie
Georg Thieme Verlag KG Stuttgart · New York

The role of aging in glucose homeostasis

C Henke
1   University Clinic Carl Gustav Carus at the TU Dresden, Medical Clinic III, DZD, Paul-Langerhans-Institute Dresden, Dresden, Germany
,
DM Willmes
1   University Clinic Carl Gustav Carus at the TU Dresden, Medical Clinic III, DZD, Paul-Langerhans-Institute Dresden, Dresden, Germany
,
A Kurzbach
1   University Clinic Carl Gustav Carus at the TU Dresden, Medical Clinic III, DZD, Paul-Langerhans-Institute Dresden, Dresden, Germany
,
T Schumann
1   University Clinic Carl Gustav Carus at the TU Dresden, Medical Clinic III, DZD, Paul-Langerhans-Institute Dresden, Dresden, Germany
,
AL Birkenfeld
1   University Clinic Carl Gustav Carus at the TU Dresden, Medical Clinic III, DZD, Paul-Langerhans-Institute Dresden, Dresden, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
05 May 2017 (online)

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    Problem:

    The prevalence of Type-2 Diabetes and insulin resistance increases with aging. Mechanisms include changes in physical activity and adiposity with aging. However, studies analyzing glucose homeostasis during aging are largely biased by an increased fat mass in old model organisms compared to young counterparts. Our study aimed to exclude this bias.

    Methods:

    Healthy young (22 weeks) C57BL/6 mice were matched for body weight and body composition to old (131 weeks) C57BL/6 mice from the same facility. Moreover, we analyzed mice in a longitudinal fashion to investigate changes within a group during their aging process.

    Results:

    Old and young mice weighed 31.36 ± 0.56 g and 31.24 ± 0.25 g respectively and did not show differences in fat mass as assessed with NMR. Surprisingly, IPGTT as well as OGTT showed improved glucose tolerance in old mice (AUC glucose [mg/dl*120 min] IPGTT 14877.5; OGTT 15317.25) compared to young mice (AUC glucose [mg/dl*120 min] IPGTT 21662.81; OGTT 25241.25; P < 0.05) along with an increase in insulin secretion during these interventions (AUC insulin [ng/ml*120 min] IPGTT 28.68 (young), 65.63 (old); OGTT 26.74 (young), 73.29 (old); P < 0.05). Similarly, glucose tolerance improved in mice studied in week 44 to 56 and week 73 to 85.

    Conclusion:

    By excluding body fat as a confounder, our data indicate that aging per se is not associated with reduced glucose tolerance in mice. In fact, in contrast to the widespread notion that aging impairs glucose homeostasis, our data rather indicate the opposite. Further studies are ongoing to analyze the underlying mechanisms.


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    No conflict of interest has been declared by the author(s).