Main achievements
1. GLP-1 increases adipose tissue capillarization and angiogenic markers, improving insulin sensitivity. Such effects involved the reduction of AGEs through the modulation of the glyoxalase system, which activity was demonstrated to be downregulated in the adipose tissue of prediabetic and diabetic patients (10.1016/j.phrs.2020.105198)
2. Visceral adipose tissue of prediabetic and diabetic patients has an imbalance in the expression of dopamine receptors, being correlated with the lower expression of the insulin receptor and lipid oxidation mechanisms. Similar results were observed in diabetic obese rats, where the treatment with the D2 receptor agonist Bromocriptine reversed such mechanisms, upregulating adipose tissue dopaminergic signalling and lipid oxidation and insulin receptor pathways. Such mechanisms improved hepatic steatosis and systemic metabolism (10.1016/j.molmet.2021.101241). We have demonstrated that dopamine directly acts in liver and adipose tissue to regulate insulin signalling, glucose uptake and lipid oxidation (10.3389/fphar.2021.713418)
3. Circulating dopamine levels are regulated by nutritional cues and act in the adipose tissue to modulate GLP-1-induced catabolic activity (10.3390/ijms24032464)
4. Exposure to maternal glycation and obesogenic environments during perinatal period impairs NPY and Dopamine receptors in the adipose tissue and liver, dysregulating glucose and lipid metabolism and leading to accumulation of liver fat (10.3390/nu15051281)
5. Several curcumin derivatives have been synthesized over the years to overcome its solubility and bioavailability problems (10.1007/s12272-020-01240-3) We have identified a new curcumin synthetic derivative for the prevention of stress outcomes, disease mechanisms and vascular function of type 2 diabetes (10.3390/ijms23105652).
Publications
Scientific interests and ongoing research projects
1. To unravel the mechanisms leading to adipose tissue dysfunction in obesity, and its relation to the development of NAFLD, hepatic insulin resistance and brain vascular and metabolic alterations throughout the life course. The aim is also to disclose the role of advanced glycation end-products (AGEs) in the development of adipose tissue insulin resistance, dysregulation of metabolic and endocrine function and impairment of tissue plasticity.
2. To develop new biomarkers of obesity-related pathologies and type 2 diabetes complications using multimodal imaging, proteomics, metabolomics, and gut signals, such as gut hormones and microbiome. This specific objective relies in the crosstalk between different biochemical and functional markers in order to achieve reliable markers of disease progression and prevent obesity and diabetes-associated morbidity.
3. To address the nutrient-sensing mechanisms governing central and peripheral modulation of energy balance (appetite and energy expenditure). The aim is to determine the crosstalk between the gut and the adipose tissue in order to identify the mechanisms involved in post-prandial nutrient sensing and storage, as well as in energy expenditure, the two main pillars of energy balance regulation. The identification of such mechanisms may identify new therapeutic targets in order to prevent obesity-related diseases and type 2 diabetes.
4. To develop innovative drugs and nutritional strategies able to prevent glycation, glucotoxicity and energy imbalance, preventing diabetic complications and regulating the gut mechanisms involved in post-prandial nutrient sensing (gut hormones and microbiome).