Normal ageing in humans, and also in rodents, is accompanied by progressive increase in adiposity, presumably caused by impaired control of energy homeostasis. Transcriptional regulation and reduced hormonal activity represent important factors in the loss of homeostasis, which may also lead to atherosclerosis.
- Atherosclerosis (Weih)
promotion of atherosclerosis by LTβR-dependent mechanisms through the alternative NF-κB pathway; inflammation as a co-factor for atherosclerosis in aged ApoE-deficient mice
- Central control of energy expenditure by thyrotropin releasing hormone (TRH) (Bauer, Heuer)
functions of TRHergic neurons as integrators of metabolic signals in mouse models
- Metabolic side effects of glucocorticoids (Tuckermann)
Excess of glucocorticoids during steroid therapy leads to fat redistribution, muscle atrophy and insulin resistance. Some of these symptoms are also developed in the metabolic syndrome. With cell type and functions selective mutant mice of the glucocorticoid receptor (GR) we unravel the cellular contribution and the molecular mechanism in these pathologies.
- Transcription factor-dependent control of energy homeostasis (Calkhoven)
role of Sirt1 and C/EBPs in the regulation of metabolic and stress genes