Members
Nicole Klas (Technician starting Oct 2026)
Our research group studies molecular mechanisms that regulate adipose tissue energy metabolism and its communication with other organs. We combine energy metabolism and nutritional biology to investigate how adipose tissue dysfunction develops during obesity and contributes to metabolic disease.
Adipose tissue is a central regulator of metabolic health. Beyond energy storage, it functions as a dynamic endocrine organ that senses nutritional and hormonal cues and communicates with other tissues. Dysfunctional adipose tissue is the primary driver of obesity-associated comorbidities: impaired plasticity, inflammation and endocrine control disrupts energy balance, insulin sensitivity, and lipid homeostasis, leading to metabolic complications linked to obesity. Understanding these processes is essential for identifying new targets to prevent and treat obesity-related diseases.
We are specifically interested to investigate molecular mechanisms to enhance adipose tissue metabolism. A key driver of obesity-induced adipose tissue dysfunction is mitochondrial dysfunction, which contributes to cellular stress, disrupted energy homeostasis, and metabolic inflexibility. Interestingly, different adipose tissue types differ markedly in their mitochondrial content and metabolic functions. Whereas white adipose tissue (WAT) primarily functions in energy storage, brown adipose tissue (BAT) dissipates chemical energy as heat and thereby contributes to whole-body energy expenditure. Importantly, adipose tissue exhibits remarkable plasticity, and some WAT depots can acquire a brown fat–like (beige) phenotype also termed “browning” of white fat. Understanding the endocrine and molecular networks that govern adipose tissue plasticity may reveal novel strategies to improve adipose tissue function and combat associated metabolic disorders.
Furthermore, our lab focuses on endocrine acting proteins as modulators of energy balance in obesity. Circulating hormones and stress-responsive signaling factors are key modulators of adipose tissue function. Here, we investigate potential synergetic actions of hormones, changes in tissue specificity and hormone resistance.
One examples of such an endocrine regulator is fibroblast growth factor 21 (FGF21). Interestingly, pharmacological administration improves adiposity and lipid profiles in rodents and humans. However, endogenous circulating levels are elevated in obesity, suggesting that obesity is associated with a state of FGF21 resistance or a compensatory upregulation of the hormone. Thus, FGF21´s endogenous physiological role and underlying molecular mechanisms remain incompletely understood. Defining these mechanisms is critical for the development of safe and effective anti-obesity therapies.
To address our specific research aims, we make use of loss- and gain-of-function models in-vitro and in-vivo, combined with metabolic phenotyping and in depth molecular characterization including RNA sequencing and plate based respirometry.