Table 1.

Four Stages of Islet Microcirculation Re-modeling in the HIP Rat Model of Type 2 Diabetes Mellitus^a

I	Quiescent stage: 2-month HIP model
	No obvious microcirculation remodeling as compared to the SDC model.
	Loss of desmosomes and adherens junctions associated with widening of the islet exocrine interface.
II	Islet wounding stage: 4-month HIP model
	Pericapillary islet amyloid deposition, islet amyloid deposition between the pericyte and endothelial cell of the microcirculation, strongest signal for α-SMA antibody positive staining of pericytes and pericyte hyperplasia and/or migration to the islet exocrine interface.
III	Pericyte and β-cell apoptosis stage: 8-month HIP model
	Pericyte and β-cell apoptosis, progressive migration and or hyperplasia of pericytes
	in the islet exocrine interface. Endocrine islet cell invasion of the exocrine extracellular matrix.
IV	Cellular - Pericyte differentiation stage: 14-month HIP model
	Adipogenesis, collagenosis and angiogenesis
	The islet microcirculation paradox: consisting of intra-islet capillary rarefaction occurring contemporaneously with islet exocrine interface angiogenesis.
	Each of the above seems to be strongly associated with the pericyte.

^aHIP, human islet amyloid polypeptide; T2DM, type 2 diabetes mellitus.