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Mechanisms and neuroanatomical bases of metabolic depression in the Djungarian hamster.

Subject Area Animal Physiology and Biochemistry
Term from 2018 to 2024
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 399844041
 
Final Report Year 2024

Final Report Abstract

Djungarian hamsters use daily torpor, a form of metabolic depression, to reduce energy expenditure when facing seasonal or acute energetic bottlenecks. The aims of this project were to (1) clarify the role of glucose, as main source of energy, in torpor regulation and to (2) identify distinct hypothalamic nuclei potentially involved in neuronal torpor control. To address, whether blood glucose levels are acutely involved in induction of spontaneous and/or fasting induced torpor, we used a novel telemetry method to continuously measure blood glucose levels, body temperature and activity in vivo over several weeks. Additionally, metabolic rate and respiratory exchange rate were determined. Our measurements demonstrated that during spontaneous daily torpor, glucose decreased in parallel with metabolic rate but before body temperature. During arousal, blood glucose increased and pretorpor values were reached at the end of the torpor bout. To our surprise and although foodrestricted hamsters under long photoperiod underwent a considerable energetic challenge, blood glucose levels remained stable during the resting phase regardless of torpor expression. The activity phase preceding a torpor bout did not reveal changes in blood glucose that might be used as torpor predictor. Gene expression data, did not indicate altered neuronal glucose transport in the hypothalamus. Dietary or pharmacological manipulations that were used to induce a (glucose-related) energy challenge resulted in a drastic metabolic shifts towards lipid metabolism. However, this neither guaranteed the expression of metabolic downstates, nor were the provoked bouts of hypometabolism and hypothermia comparable to spontaneous torpor. Hence, our measurements could show that blood glucose is not a proximate torpor induction factor, neither of spontaneous torpor in short-photoperiod acclimated nor of fasting induced torpor in long-photoperiod acclimated Djungarian hamsters. In the second part of the project, we aimed to identify distinct hypothalamic nuclei potentially involved in torpor control. Transcriptomics of whole hypothalamus found substantial gene expression changes during torpor, but do not give precise enough anatomic information to allow identification of specific mechanism. Here, we used expression of the immediate early gene c-Fos to identify transcriptionally active hypothalamic areas over the course of a torpor bout followed by nucleus-specific next generation sequencing to narrow down their functional relevance. Only one hypothalamic structure showed distinct and differential c-Fos expression during torpor, namely the suprachiasmatic nucleus, comprising the circadian clock. Subsequently, we used laser capture microdissection to dissect the suprachiasmatic nucleus, as well as the paraventricular nucleus as well-known clock output, during torpor entry and arousal. Reactome pathway analyses revealed an overrepresented mitochondrial translation driven by genes upregulated during entry in SCN and an overrepresented transcription driven by downregulated genes during arousal in SCN as well as PVN. Our results support the hypothesis, that the SCN maintains cellular activity during torpor and is actively involved in torpor control. SCN function and signalling during daily torpor is a promising route for follow up studies.

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