Research

Environmental Pollutants & Metabolic Disruption 

We investigate how environmental pollutants enter biological systems and interfere with metabolic homeostasis — disrupting hormonal signaling, inflammatory balance, glucose & fat metabolism and energy regulation at the molecular and systemic level.

Our research covers:

• Micro- and Nanoplastics (MNPs) — disruption of insulin signaling (IRS-1/AKT/GLUT4), lipid metabolism, and glucose homeostasis; cellular internalization, oxidative stress induction, and gut-metabolic axis interference

• Particulate Matter (PM₁₀) — inflammatory activation via NF-κB and NLRP3 inflammasome, mitochondrial stress, and systemic metabolic dysregulation linked to obesity and T2D risk

• Persistent Organic Pollutants (POPs) — obesogenic/diabetogenic mechanisms including altered lipid storage and pancreatic β-cell toxicity

• Endocrine-Disrupting Chemicals (EDCs) — interference with nuclear receptor signaling (PPARγ) driving adipogenesis, thyroid dysfunction, and insulin resistance

Lifestyle, Diet & Metabolic Disease: The Metabolic Cost of Modern Life

Unhealthy dietary patterns are among the leading drivers of metabolic disease. We model and investigate how diet-induced metabolic stress mirrors and interacts with pollutant-induced dysfunction — spanning cellular, and systemic levels.

Our research covers:

High-fat and high-glucose diets (HFD/HG) — obesity, insulin resistance, dyslipidemia, and the progression from simple steatosis to NAFLD, MASH (metabolic dysfunction-associated steatohepatitis), and MASL (metabolic dysfunction-associated steatotic liver disease)

Diet-induced liver disease — mechanisms driving hepatic lipid accumulation, inflammation, fibrosis, and the NAFLD→MASH continuum

Intermittent fasting and caloric restriction — metabolic reprogramming, energy sensing (AMPK, mTOR, SIRT1), and protective mechanisms against obesity, T2D, and fatty liver disease

Diet–pollutant interactions — how dietary metabolic stress amplifies or modifies toxicant-induced metabolic dysfunction

Insulin Resistance & Metabolic Signaling

At the core of our research is understanding the molecular basis of insulin resistance — across both pollutant-exposed and diet-induced models — and how disrupted signaling cascades drive systemic metabolic disease.

Our research covers:

Insulin signaling pathway disruption 

Inflammatory crosstalk 

Lipotoxicity and ectopic fat accumulation

Mitochondrial dysfunction 

Adipokine and hepatokine dysregulation 

Crosstalk between pollutant- and diet-induced models