S K Sreenan

Deppartment of Medicine, the University of Chicago, Chicago, Illinois, USA.

3 publications 1998 – 2001

What does S K Sreenan research?

S K Sreenan studies the role of certain proteins and genetic factors in how the body produces and uses insulin, a hormone vital for controlling blood sugar levels. Their research specifically looks at conditions related to diabetes, particularly type 2 diabetes, and how pancreatic cells respond to high sugar levels. By examining how blocking certain proteins can impact insulin release and how defects in glucose-sensing genes can lead to improved insulin response, Sreenan sheds light on the complexities of blood sugar management in the body.

Key findings

  • Blocking calpain proteins leads to increased insulin release from the pancreas in response to high blood sugar, while making muscle and fat cells less responsive to insulin's signals.
  • In glucokinase mutant mice, exposure to high blood sugar for 2-4 days resulted in enhanced insulin secretion, highlighting an adaptation that allows defective cells to partially overcome their limitations.
  • Normal pancreatic cells exhibit decreased function under prolonged high blood sugar, contrasting with the adaptive response seen in defective cells, which helps explain the stable blood sugar levels in individuals with glucokinase mutations.

Frequently asked questions

Does Dr. Sreenan study diabetes?
Yes, Dr. Sreenan's research focuses on type 2 diabetes and how the body responds to high blood sugar.
What treatments has Dr. Sreenan researched?
Dr. Sreenan's work involves understanding insulin secretion mechanisms and the impact of certain proteins, which may contribute to future treatments for diabetes.
Is Dr. Sreenan's work relevant to patients with high blood sugar?
Absolutely, their research addresses how the body manages high blood sugar, which is crucial for patients with diabetes.
What is the role of calpains in insulin production?
Calpains are proteins that, when blocked, can lead to increased insulin release from the pancreas.
How do glucokinase mutations affect blood sugar levels?
Mutations in the glucokinase gene can lead to milder, stable high blood sugar because these defective cells adapt to prolonged sugar exposure.

Publications in plain English

Calpains play a role in insulin secretion and action.

2001

Diabetes

Sreenan SK, Zhou YP, Otani K, Hansen PA, Currie KP +11 more

Plain English
Researchers found that blocking calpain proteins—which are found throughout the body—causes pancreases to release more insulin in response to high blood sugar, and simultaneously makes muscles and fat cells less responsive to insulin's signals. Since genetic variations in the calpain-10 gene are linked to type 2 diabetes, these results suggest that calpains are a key control point for how much insulin the body makes and how well cells use it.

PubMed

Glucagon-like peptide-1 stimulates insulin secretion by a Ca2+-independent mechanism in Zucker diabetic fatty rat islets of Langerhans.

2000

Metabolism: clinical and experimental

Sreenan SK, Mittal AA, Dralyuk F, Pugh WL, Polonsky KS +1 more

Plain English
This study looked at how a hormone called glucagon-like peptide-1 (GLP-1) affects insulin release in two types of rats: diabetic Zucker fatty rats and their lean counterparts. The researchers found that while the lean rats responded to GLP-1 and increased insulin secretion when glucose levels were high, the diabetic rats didn't show a significant response to glucose but did increase insulin secretion when exposed to GLP-1. This difference is essential because it helps us understand how insulin release works differently in diabetic conditions, which can inform treatment strategies for diabetes. Who this helps: This information is valuable for doctors treating diabetic patients.

PubMed

Adaptation to hyperglycemia enhances insulin secretion in glucokinase mutant mice.

1998

Diabetes

Sreenan SK, Cockburn BN, Baldwin AC, Ostrega DM, Levisetti M +5 more

Plain English
Researchers studied pancreatic cells from mice with a broken glucokinase gene (a gene that helps detect blood sugar) to see if exposing them to high blood sugar would improve their ability to make insulin. They found that cells from mutant mice actually recovered function when exposed to high sugar levels—they produced more insulin and better detected blood sugar changes—while normal cells exposed to the same high sugar levels became damaged and stopped working properly. This matters because it explains why people with glucokinase gene mutations don't develop severe diabetes: their pancreatic cells adapt to high blood sugar instead of breaking down, and it suggests that having only one working copy of this gene actually provides protection against the cell damage that normally happens when blood sugar stays too high.

PubMed

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