Robert K. Baker

Cellular reprogramming of human amniotic fluid cells to express insulin.

IGFBP2 is neither sufficient nor necessary for the physiological actions of leptin on glucose homeostasis in male ob/ob mice.

Overexpression of PPARγ specifically in pancreatic β-cells exacerbates obesity-induced glucose intolerance, reduces β-cell mass, and alters islet lipid metabolism in male mice.

Overexpression of PAX4 reduces glucagon expression in differentiating hESCs.

FGF21-Mediated Improvements in Glucose Clearance Require Uncoupling Protein 1.

The Role of ARX in Human Pancreatic Endocrine Specification.

Leptin contributes to the beneficial effects of insulin treatment in streptozotocin-diabetic male mice.

Metabolic effects of leptin receptor knockdown or reconstitution in adipose tissues.

AAV GCG-EGFP, a new tool to identify glucagon-secreting α-cells.

SNAP23 depletion enables more SNAP25/calcium channel excitosome formation to increase insulin exocytosis in type 2 diabetes.

AAV8 Ins1-Cre can produce efficient β-cell recombination but requires consideration of off-target effects.

Role of myeloid cell leptin signaling in the regulation of glucose metabolism.

Deletion of pancreas-specific miR-216a reduces beta-cell mass and inhibits pancreatic cancer progression in mice.

Insulin Null β-cells Have a Prohormone Processing Defect That Is Not Reversed by AAV Rescue of Proinsulin Expression.

The Impact of Different Implantation Sites and Sex on the Differentiation of Human Pancreatic Endoderm Cells Into Insulin-Secreting Cells In Vivo.

Protocol development to further differentiate and transition stem cell-derived pancreatic progenitors from a monolayer into endocrine cells in suspension culture.

Differentiation of stem cell-derived pancreatic progenitors into insulin-secreting islet clusters in a multiwell-based static 3D culture system.