I head the MEtabolic DIseases Research (MEDIR) group which is committed simultaneously in establishing an integrated picture of the etiological processes that determine the development of prediabetes, diabetes. I supervised 16 concluded PhDs (6 ongoing), all followed a post-doctoral formation, 6 are pursuing their carriers as scientific investigators (academic, clinic and private). The incorporation of clinician scientists in the MEDIR group warrants the translation into the clinics. The unique close relationship with APDP diabetes Portugal, the oldest patient association in the world and one of the biggest outpatient clinics exclusively dedicated to diabetes, allows an exceptional scientific environment which aims at early-detecting, biomarkers for disease stratification and design new precision medicine approaches.

In the early times as a PI I dedicate my scientific career to prediabetes/diabetes addressing the hypothesis that its etiology is diverse. My first approach was to understand the subcluster of people that had impaired postprandial glucose homeostasis. In this field I made advance in significance of the autonomic nervous system in the control of postprandial glucose homeostasis. More recently, I examine the overarching hypothesis that hepatic subclinical inflammatory states, derived from diet-induced changes in intestinal microbiota, originates a sustained suppression on hepatic insulin clearance leading to persistent hyperinsulinemia, as the liver is responsible for 50-70% of the insulin clearance. In turn, this primary hyperinsulinemia leads to insulin resistance resulting in mild hyperglycemia against which the pancreas responds by increasing insulin secretion and thereby escalating the hyperinsulinemic state and insulin resistance. Even though at a first glance the obvious axis is between the gut and the liver we discover that the paraventricular nucleus of the hypothalamus also controls insulin clearance. Newly, by pinpointing my understanding that clustering Type 2 Diabetes based on comorbidities/complications are urgently needed for precision medicine I recently embraced a novel strategy for deep phenotyping based not only on organ disease state but also on organ communication. Precison medicine has frankly evolved in cancer field. Learning from it I have been working in the hypothesis that exosomes can stratify T2D, apprise on organ disease status as each organ appear to have a specific exosome signature, and to inform on organ communication since exosomes appear to have specific ZIP codes for this propose which when its cargo is disrupted can impinge on a pathological state.