Medical research

Enhanced autophagy could help treat diabetes

Enhancing autophagy—the cellular process that breaks down and removes unneeded components—in fat tissue could help treat diabetes, according to a Northwestern Medicine study published in Cell Reports.

Biomedical technology

Engineering diseased human skin in vitro

The skin, which covers the surface of the human body, is its largest organ. It is the first organ to show changes stemming from organ or physiological activity. It is especially common for diabetic patients to suffer from ...

Medical research

Researchers identify muscle factor that controls fat metabolism

Metabolic diseases, such as obesity and type 2 diabetes, have risen to epidemic proportions in the U.S. and occur in about 30 percent of the population. Skeletal muscle plays a prominent role in controlling the body's glucose ...

page 1 from 40

Insulin resistance

Insulin resistance (IR) is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. Insulin resistance in fat cells reduces the effects of insulin and results in elevated hydrolysis of stored triglycerides in the absence of measures which either increase insulin sensitivity or which provide additional insulin. Increased mobilization of stored lipids in these cells elevates free fatty acids in the blood plasma. Insulin resistance in muscle cells reduces glucose uptake (and so local storage of glucose as glycogen), whereas insulin resistance in liver cells results in impaired glycogen synthesis and a failure to suppress glucose production. Elevated blood fatty acid levels (associated with insulin resistance and diabetes mellitus Type 2), reduced muscle glucose uptake, and increased liver glucose production all contribute to elevated blood glucose levels. High plasma levels of insulin and glucose due to insulin resistance are believed to be the origin of metabolic syndrome and type 2 diabetes, including its complications.

This text uses material from Wikipedia, licensed under CC BY-SA