Sandra Kristine Stølen Bryne

• Dufour, Damien; Bryne, Sandra Kristine Stølen; Dapsance, Florian; Ferrito, Noemi; Plotton, Ingrid & Dalen, Knut Tomas [Show all 9 contributors for this article] (2025). Mechanisms of sexually dimorphic adipose tissue remodelling upon prolonged breastfeeding. bioRxiv (preprint article). doi: 10.1101/2025.09.05.674416. Full text in Research Archive Show summary

  Early developmental cues exert lasting influence on the adipose tissue function and the metabolic health throughout adulthood. In mice, adipose tissue remodelling during the weaning transition programs long-term tissue plasticity, setting its capacity for expansion and thermogenesis in response to environmental stimuli. However, the mechanisms driving this remodelling, and the role of weaning-associated dietary changes in this process, are unknown. Here, we characterise the emergence of sexually dimorphic patterns of adipose tissue distribution and function during the post-weaning period. As subcutaneous adipocytes acquire a white phenotype, the tissue microenvironment undergoes a coordinated remodelling, including reduced innervation and an increase in immune cell content. Using a model of prolonged breastfeeding, we show that it promotes adipose tissue expansion through sex-dependent mechanisms, stimulating progenitor proliferation in males and adipocyte hypertrophy in females. In males, this is accompanied by accelerated tissue whitening, which we link to enhanced clearance of extracellular noradrenaline by mature adipocytes. Our findings reveal sex- and diet-dependent mechanisms governing adipose tissue maturation and highlight how early life nutritional cues shape the microenvironment and function of mature adipocytes. Highlights - The peri-weaning period associates with sexually dimorphic remodelling of the adipose tissue - Whitening of the adipose tissue associates with immune infiltration and decrease innervation in both sexes - Prolonged breastfeeding prevents drop in proliferation in males - Whitening is accelerated in males during prolonged breastfeeding

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• Bryne, Sandra Kristine Stølen; Dufour, Damien; Briand, Nolwenn & Boccara, Charlotte (2025). Does poor sleep during adolescence lead to metabolic disorders later in life? – Targeted chemogenetic models of sleep deprivation in mice. Full text in Research Archive Show summary

  Poor sleep and obesity are concurrent health epidemics in adolescents. This is especially concerning given that adolescents are getting less and less sleep as technology invades their bedrooms. Several studies point to adolescence as a critical period for sleep and adipose tissue development, implying that poor sleep during this period might alter the normal development of adipose tissue and cause metabolic imbalance. To investigate whether adolescent sleep quality contributes to the emergence of metabolic dysfunctions later in life, we propose to establish new rodent models of reversible sleep deprivation for which we can turn on and off sleep quality/quantity at specific developmental windows. Here we present preliminary data of our new chemogenetic model for which we can disturb sleep at specific time points between postnatal day P21 and P54 by targeting brain nuclei promoting wakefulness through the stimulation of GABAergic neurons in the ventral pallidum. We assessed the sleep amounts and quality of these animals by recording their neural (EEG) and muscular (EMG) activity. Metabolic parameters during and after sleep disturbances were assessed with metabolic cages (energy expenditure, respiratory exchange rate, food intake, weight, activity), adipose tissue histology and plasma collection (hormones and proteins). Our preliminary results indicate successful sleep deprivation concomitant with decreased respiratory exchange rate indicating a shift toward lipid oxidation as a primary energy source.

• Bryne, Sandra Kristine Stølen; Dufour, Damien; Briand, Nolwenn & Boccara, Charlotte (2025). Can poor sleep during adolescence lead to metabolic disorders later in life?- Targeted chemogenetic models of sleep deprivation in mice. Full text in Research Archive Show summary

  Obesity and poor sleep are concurrent health epidemics in adolescents. This is especially concerning given that adolescents are getting less and less sleep as technology invades their bedrooms. Several studies point to adolescence as a critical period for sleep and adipose tissue development, implying that poor sleep during this period might alter the normal development of adipose tissue. To investigate whether adolescent sleep quality contributes to the emergence of metabolic dysfunctions later in life, we propose to establish new rodent models of reversible sleep deprivation for which we can turn on/off sleep quality/quantity at specific developmental windows. Here we present preliminary data of our new chemogenetic model for which we can disturb sleep at specific time points between postnatal day P21 and P54 by targeting brain nuclei promoting wakefulness through the stimulation of GABAergic neurons in the ventral pallidum. We assessed the sleep amounts and quality of these animals by recording their neural (EEG) and muscular (EMG) activity. Metabolic parameters during and after sleep disturbances were assessed with metabolic cages (energy expenditure, respiratory exchange rate, food/water intake, weight), adipose tissue histology and plasma collection (hormones and proteins). Our preliminary results indicate successful sleep deprivation concomitant with decreased respiratory exchange rate indicating a shift toward lipid oxidation as a primary energy source.

• Bryne, Sandra Kristine Stølen; Dufour, Damien; Briand, Nolwenn & Boccara, Charlotte (2024). Inducible mouse models of adolescent sleep deprivation: the role of sleep in metabolic health. Full text in Research Archive

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