New evidence suggests that cellular organelles such as endoplasmic reticulum, mitochondria, and lysosomes—already recognized as important in beta-cell function—are active communicators using newly recognized intra- and intercellular channels.

“Organelles are providing important functions beyond what people have anticipated, like making new proteins in the endoplasmic reticulum or making ATP (adenosine triphosphate) for energy in the mitochondria,” said Ling Qi, PhD, Professor of Molecular and Integrative Physiology at the University of Michigan Medical School. “Their function goes far beyond these recognized areas. We are just scratching the surface of communications between these organelles, and it clearly plays important roles in the function of beta cells and the course of diabetes.”

Dr. Qi will discuss some of the latest research in this area during Tuesday’s symposium Beta-Cell Organelles Talk Amongst Themselves, which will begin at 7:30 a.m. in S-303 (South, Level 3).

Organelle crosstalk is important in the function and dysfunction in beta cells, added Amelia K. Linnemann, PhD, Assistant Professor at the Herman B. Wells Center for Pediatric Research and the Center for Diabetes and Metabolic Diseases at Indiana University.

“Intrinsic communication within beta cells is important in how they respond to stress, or in an environment of increased risk for diabetes development,” Dr. Linnemann said. “Communication between organelles is part of vesicle biogenesis and transport of insulin to the cell membrane, which is critical for insulin secretion. It’s also important in autophagy, a mechanism to break down dysfunctional proteins within the cell that plays a key role in beta-cell homeostasis.”

Dr. Linnemann is investigating the basic mechanisms of autophagy in type 1 diabetes. Beta-cell autophagy is an active area of research, she said, but largely in type 2 diabetes.

“The concept that these basic biological processes play a key role in beta-cell survival, dysfunction, and disease processes and could play a role in the pathogenesis of diabetes is a novel aspect,” she said. “Especially in the type 1 realm, the contributions of beta-cell dysfunction to disease initiation are becoming much better appreciated.”

It’s possible that some beta-cell dysfunction may result from the breakdown of intracellular communication channels between organelles within beta cells. Dr. Qi’s research focuses on endoplasmic reticulum (ER) function and dysfunction. The endoplasmic reticulum is responsible for protein folding and maturation and appears to play a vital role in proper functioning of other organelles. An accumulation of misfolded proteins and protein aggregates is a key determinant of many human diseases, including diabetes.

“We think that improving ER protein maturation can improve mitochondrial function and other organelle function as well,” Dr. Qi said. “We are trying to understand how this process can be targeted for both type 1 and type 2 diabetes. This symposium will provide some fundamental insights into organelle biology in diabetes and in the function of beta cells.”