- Characterizing the mechanisms of action and cell specificity underlying the anti-diabetic actions of lanthionine synthetase C-like 2 (LANCL2).
- Developing and refining novel animal models of type 2 diabetes and obesity.
- Characterizing novel classes of naturally occurring compounds with anti-diabetic and anti-inflammatory properties.
- Applying computational and mathematical modeling to integrate data and conceptual frameworks related to inflammatory and metabolic processes associated with type 2 diabetes. For instance modeling can be used to integrate metabolic and immunological data types.
- Apply bioinformatics and networks analyses approaches to identify novel therapeutic targets for metabolic and chronic inflammatory diseases.
- Investigating the cross-talk between immunity and metabolism in animal models that combine metabolic disease and infection.
Chronic diseases include metabolic inflammatory conditions such as obesity, diabetes, and cardiovascular disease. The NIMML is identifying and validating novel therapeutic targets for the treatment of obesity-related co-morbidities such as type-2 diabetes and developing lead compounds that can modulate these novel targets. Low-grade chronic inflammation is associated with overweight and obesity, type-2 diabetes and cardiovascular disease. The NIMML is identifying and validating novel therapeutic targets for the treatment of type-2 diabetes, and developing lead compounds that can modulate these novel targets.
Lanthionine synthetase component C-like protein 2: a new drug target for inflammatory diseases and diabetes.
Elevated CD8 T cell responses in type 1 diabetes patients to a 13 amino acid coeliac-active peptide from α-gliadin.
Treatment of Obesity-Related Complications with Novel Classes of Naturally Occurring PPAR Agonists.
Abscisic acid regulates inflammation via ligand-binding domain-independent activation of peroxisome proliferator-activated receptor gamma.
Gene regulatory network reveals oxidative stress as the underlying molecular mechanism of type 2 diabetes and hypertension.
Molecular modeling of lanthionine synthetase component C-like protein 2: a potential target for the discovery of novel type 2 diabetes prophylactics and therapeutics.
Genistein induces pancreatic beta-cell proliferation through activation of multiple signaling pathways and prevents insulin-deficient diabetes in mice.
Abscisic acid ameliorates experimental IBD by downregulating cellular adhesion molecule expression and suppressing immune cell infiltration.
Abscisic acid synergizes with rosiglitazone to improve glucose tolerance and down-modulate macrophage accumulation in adipose tissue: possible action of the cAMP/PKA/PPAR γ axis.
Mechanisms of action and medicinal applications of abscisic Acid.
Activation of PPAR gamma and alpha by punicic acid ameliorates glucose tolerance and suppresses obesity-related inflammation.
Virtual Screening as a Technique for PPAR Modulator Discovery.
Catalpic acid decreases abdominal fat deposition, improves glucose homeostasis and upregulates PPAR alpha expression in adipose tissue.
Dietary modulators of peroxisome proliferator-activated receptors: implications for the prevention and treatment of metabolic syndrome.
Putting the pieces of the puzzle together - a series of hypotheses on the etiology and pathogenesis of type 1 diabetes.
Dietary abscisic acid ameliorates glucose tolerance and obesity-related inflammation in db/db mice fed high-fat diets.