Category: Beta Cell Physiology and Dysfunction

Type 2 diabetes (T2D) increases with age with the majority of patients being above the fifth decade of life. These data underline the importance of studying how aging contributes to the reduced beta cell mass and dysfunctional insulin secretion found in T2D. However, the specific contribution of beta cell aging and senescence to diabetes has […]

Two major pathophysiologic abnormalities underlie most cases of type 2 diabetes (T2D): insulin resistance and defects in pancreatic beta-cell function. These defects are initially compensated by an increase in insulin secretion and in the number of insulin secreting cells. However, with time, beta cell dysfunction and T2D develops, requiring intervention therapies. Eventually, there is significant […]

Calcium plays a vital role in many processes that govern beta cell function, including the production, maturation, and regulated secretion of insulin. The fidelity of these processes depends on the maintenance of calcium subcompartments and their respective transmembrane gradients, which are organized at both the cellular and organelle level. Then endoplasmic reticulum, Golgi apparatus, and […]

Therapies focused on sustaining or promoting endogenous insulin production for individuals at risk for or with T1D will require a thorough understanding of the gene expression patterns in islet α, β, and δ cells from control subjects and from individuals with T1D. Toward that end, we have developed methods to essentially purify α, β, and δ cells from human pancreata by […]

We hypothesize that β-cell toxicity in T1D can be induced via different pathways by distinct pathological ligands (AGEs, S100-proteins, amyloidogenic amylin) of the receptor for advanced glycation endproducts (RAGE) that become upregulated in the diabetic pancreas. We also hypothesize that C-peptide (+) T1D subjects may be more susceptible to amylin-induced β-cell toxicity. Amylin is co-produced /co-secreted with […]