Research

Obesity is one of the most pressing global health challenges, substantially increasing the risk of type 2 diabetes, cardiovascular disease, and premature mortality. A central biological feature underlying obesity-related metabolic dysfunction is impaired mitochondrial function together with chronic low-grade inflammation in adipose tissue. These alterations disrupt adipose tissue function and contribute to metabolic complications in other organs.

Our research addresses fundamental questions related to how molecular and cellular pathways in adipose tissue and other peripheral tissues are altered in obesity, and how these pathways adapt in response to weight loss. We aim to better understand the mechanisms that support metabolic improvement and tissue remodeling during successful weight reduction.

To address these questions, we study metabolic factors in adipose tissue and circulation that change following bariatric surgery, currently the most effective and durable treatment for obesity and its metabolic complications. In particular, post-surgical increases in bile acids, gut hormones, and other circulating metabolites have been proposed to contribute to the systemic metabolic benefits of surgery by signaling to peripheral tissues. However, in humans, the relevant receptors, downstream pathways, and tissue-specific responses to these signals remain incompletely defined.

By integrating human clinical data with tissue-based and cell-based experimental approaches, our work aims to provide mechanistic insight into how adipose tissue metabolism, mitochondrial function, inflammation, and inter-organ communication are regulated in health, obesity, and during weight loss.

Human adipose tissue mitochondrial metabolism after weight loss

We study how bariatric surgery and lifestyle-based weight loss interventions affect mitochondrial metabolism in human adipose tissue and cultured human adipocytes.

Bile acids, gut hormones, and circulating metabolites in adipose tissue metabolism

We investigate the role of bile acids, gut hormones, and postprandial metabolites in regulating adipocyte function in humans. This includes studying their signaling pathways, receptor-mediated effects, and their potential role in adipose tissue–to–organ communication through metabolites and extracellular vesicles.

Mitochondrial–inflammatory interactions in adipocytes

We examine how mitochondrial activity influences inflammatory responses in adipocytes and how changes in mitochondrial function relate to adipose tissue inflammation.

Mitochondrial fuel utilization pathways in human adipocytes

We explore metabolic pathways governing substrate utilization and mitochondrial fuel oxidation in cultured human adipocytes, with the aim of understanding key aspects of adipocyte dysfunction.

Impact of type 2 diabetes on adipose tissue metabolism and postprandial responses

We study how type 2 diabetes modifies adipose tissue metabolism, postprandial metabolite responses, and metabolic adaptation during weight loss in humans.

Eating behavior after bariatric surgery or lifestyle interventions

In addition to metabolic regulation, we investigate behavioral factors associated with successful weight loss, including changes in eating behavior following bariatric surgery or lifestyle interventions.