Lung disease may increase risk of insulin resistance, diabetes, mouse study suggests

September 30, 2015, American Physiological Society

Numerous studies have identified obesity and poor diet as risk factors for insulin resistance and diabetes. A new study adds another risk factor to the list: inflammatory lung disease. Published in the American Journal of Physiology—Regulatory, Integrative and Comparative Physiology, the study reports that inflammation in the lungs is enough to induce the body-wide inflammation that can lead to insulin resistance.

Individuals with inflammatory lung diseases, such as asthma and pneumonia, frequently have high blood glucose (sugar) levels and show insulin resistance. However, these individuals often also have conditions such as obesity or steroid treatment that predispose them to risk factors of diabetes. Researchers at Vanderbilt University sought to determine if having only lung disease could increase the likelihood of developing diabetes risk factors.

The researchers observed that mice with also developed inflammation in the liver and other organs. Although in these mice was normal, insulin was less effective in controlling blood sugar: Insulin did not suppress glucose production by the liver, and was moderately impaired in other organs. The mice had signs of insulin resistance, demonstrating that inflammation in the lungs can contribute to insulin resistance and high blood sugar, according to the researchers. Therapies that reduce lung inflammation to treat lung injuries may have the additional benefit of lowering the risk of body-wide inflammation and insulin resistance, the researchers wrote.

The study "NF-κB-dependent airway inflammation triggers systemic " is published ahead of print in the American Journal of Physiology—Regulatory, Integrative and Comparative Physiology.

Explore further: Researchers find out why polycystic ovary syndrome and diabetes are linked

More information: "NF-κB Dependent Airway Inflammation Triggers Systemic Insulin Resistance." American Journal of Physiology - Regulatory, Integrative and Comparative Physiology Published 16 September 2015 Vol. no. , DOI: 10.1152/ajpregu.00442.2014

Related Stories

Researchers find out why polycystic ovary syndrome and diabetes are linked

June 4, 2015
Nearly 50 percent of women with polycystic ovary syndrome (PCOS) develop pre-diabetes or type 2 diabetes before the age of 40, but the reasons for the correlation was unclear. In a new study in the American Journal of Physiology–Endocrinology ...

Novel mechanism of insulin resistance in type 2 diabetes

September 17, 2015
Insensitivity to insulin, also called insulin resistance, is associated with type 2 diabetes and affects several cell types and organs in the body. Now, scientists from Sweden's Karolinska Institutet have discovered a mechanism ...

Insulin resistance linked to a human gene variant

March 23, 2015
Insulin resistance is a risk factor for developing both type 2 diabetes and cardiovascular disease. Almost one third of the U.S. population has some degree of insulin resistance, though it is undiagnosed in many of these ...

Research team identifies link between inflammation and type 2 diabetes

February 5, 2015
A Yale-led research team has identified the molecular mechanism by which insulin normally inhibits production of glucose by the liver and why this process stops working in patients with type 2 diabetes, leading to hyperglycemia.

Gamma-Delta T cells may play a role in insulin resistance and type 2 diabetes

January 5, 2015
New research in mice suggests that an unusual type of immune cell called "γδ T cells" may be a new drug and research target for treating or preventing type 2 diabetes caused by obesity. The research report, appearing in ...

Improving obesity-induced insulin sensitivity

June 1, 2012
In recent years, a growing body of evidence has linked inflammation to the development of insulin resistance. In insulin resistance, the hormone insulin is less effective in promoting glucose uptake from the bloodstream into ...

Recommended for you

Fat tissue may play a crucial role in the progression of diabetes, challenging long established notions

October 12, 2018
A new study by Australian researchers, out today, is challenging what we know about the causes of diabetes. The new research points to fat tissue as a source of disease, and widens our understanding beyond the traditional ...

Does breastfeeding hormone protect against type 2 diabetes?

October 12, 2018
(HealthDay)—The hormone prolactin—most commonly associated with breastfeeding—may play a role in reducing the risk of type 2 diabetes, a new study suggests.

Planned intermittent fasting may help reverse type 2 diabetes, suggest doctors

October 10, 2018
Planned intermittent fasting may help to reverse type 2 diabetes, suggest doctors writing in the journal BMJ Case Reports after three patients in their care, who did this, were able to cut out the need for insulin treatment ...

Markers of dairy fat consumption linked to lower risk of type two diabetes

October 10, 2018
Higher levels of biomarkers of dairy fat consumption are associated with a lower risk of developing type 2 diabetes, according to new research published today in PLOS Medicine. The study, in more than 60,000 adults, was undertaken ...

New discovery restores insulin cell function in type 2 diabetes

October 8, 2018
By blocking a protein, VDAC1, in the insulin-producing beta cells, it is possible to restore their normal function in case of type 2 diabetes. In preclinical experiments, the researchers behind a new study have also shown ...

Weight loss drug shows positive effect on diabetes

October 4, 2018
At the 2018 Meeting of the European Association for the Study of Diabetes, Brigham and Women's Hospital investigators from the Thrombolysis in Myocardial Infarction (TIMI) Study Group presented diabetes-related findings from ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.