Jacob T Bartosiak

Department of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.

3 publications 2018 – 2025

What does Jacob T Bartosiak research?

Jacob T Bartosiak studies how insulin-producing cells, known as beta cells, protect themselves from damage caused by palmitate, a type of saturated fat. He investigates the role of a protein called Cation-Independent Mannose 6-Phosphate Receptor (CI-MPR) in these cells. His research aims to reveal how maintaining a cell's waste-disposal system helps prevent damage, which is crucial for crafting better treatments for conditions like type 2 diabetes.

Key findings

  • Cells that lack the CI-MPR protein are extremely vulnerable to damage from palmitate, leading to impaired insulin production.
  • Maintaining the function of the cell's waste-disposal system is a key factor in protecting beta cells from fatty acid damage.
  • The research indicates potential new treatment strategies for type 2 diabetes by enhancing the ability of insulin-producing cells to withstand fatty acid exposure.

Frequently asked questions

Does Dr. Bartosiak study diabetes?
Yes, Dr. Bartosiak focuses on diabetes, particularly how insulin-producing cells are affected by fatty acids like palmitate.
What treatments has Dr. Bartosiak researched?
He is exploring ways to protect insulin-producing cells from damage, which could lead to new treatments for type 2 diabetes.
Is Dr. Bartosiak's work relevant to patients with type 2 diabetes?
Yes, his research is directly relevant as it seeks to improve the health and function of insulin-producing cells, which are critical in type 2 diabetes management.

Publications in plain English

Lipopolysaccharide-induced cytokine signaling activates a temporal innate defense program and represses pancreatic β-cell identity.

2025

The Journal of biological chemistry

Bartosiak JT, Hansen PA, Schumacher EA, Harty KR, Stancill JS +1 more

Plain English
This study looked at how cytokines, which are signaling molecules involved in immune responses, affect insulin-producing cells in the pancreas during an immune reaction triggered by a bacterial component. Researchers found that these cytokines quickly activate protective genes while reducing the factors that define pancreatic beta cells, but this effect only lasts about 24 hours. Understanding this process is important because it shows how the body can protect these crucial insulin-producing cells during infections rather than just focusing on the negative impacts of cytokines in diabetes. Who this helps: This research benefits patients with type 1 diabetes and their doctors by providing insights into how to better protect insulin-producing cells.

PubMed

Cholecystokinin attenuates β-cell apoptosis in both mouse and human islets.

2022

Translational research : the journal of laboratory and clinical medicine

Kim HT, Desouza AH, Umhoefer H, Han J, Anzia L +8 more

Plain English
This study looked at a hormone called cholecystokinin (CCK) and its effects on pancreatic beta cells, which are crucial for insulin production in diabetes. The researchers found that CCK can significantly reduce cell death caused by inflammatory signals in both mouse and human pancreatic cells; specifically, CCK treatment decreased beta-cell death in human islets and in diabetic mice. This finding is important because it offers a potential new treatment to help preserve insulin-producing cells, which could lead to better outcomes for people with diabetes, especially after islet transplants. Who this helps: This research benefits patients with type 1 and type 2 diabetes, particularly those undergoing islet transplantation.

PubMed

Cation-Independent Mannose 6-Phosphate Receptor Deficiency Enhances β-Cell Susceptibility to Palmitate.

2018

Molecular and cellular biology

Baldwin AC, Naatz A, Bohnsack RN, Bartosiak JT, Oleson BJ +3 more

Plain English
Researchers discovered that insulin-producing cells protect themselves from damage caused by palmitate (a common fatty acid) by using a cellular cleanup system called lysosomes to break down and remove damaged proteins. Cells that lacked a specific protein needed to deliver garbage to lysosomes were much more vulnerable to palmitate damage, while cells with this protein intact survived better. This finding suggests that keeping the lysosomal cleanup system working properly is essential for pancreatic cells to survive when exposed to excess fat.

PubMed

Publication data sourced from PubMed . Plain-English summaries generated by AI. Not medical advice.