Presentation Title

DAIRY DERIVED FATTY ACIDS IMPACT PANCREATIC BETA CELL FUNCTION

Presenter's Name(s)

James B. Whitley, UVMFollow

Project Collaborators

Thomas Jetton and Jana Kraft (Thesis Mentors)

Abstract

Epidemiological studies have established that full-fat dairy consumption reduces the risk of type 2 diabetes (T2D) development, particularly, the dairy-derived fatty acid trans-palmitoleic acid (16:1; TPA), although the underlying mechanisms are unknown. Recently, it has been found that 15-methyl-hexadecanoic acid (iso 17:0; MHA) may also be responsible for these effects. Since the insulin-secreting pancreatic beta cell is dysfunctional in T2D, the goal of this project was to evaluate whether TPA and MHA directly impact glucose induced insulin secretion (GIIS) in an in vitro model. The objectives of this study were to 1) determine the extent to which GIIS is influenced following short-term exposure to MHA or TPA as compared to palmitic acid (PA, a control fatty acid (FA)) in normal cultured rat pancreatic islets (microscopic structures comprised mostly of beta cells), and 2) determine the extent to which GIIS is impacted by long-term exposure to MHA or TPA in culture conditions mimicking a T2D environment. Whereas TPA, MHA, and PA short-term incubated islets in the presence of basal glucose had no significant effect on GIIS, in the presence of high glucose, GIIS was augmented 1.72-, 1.24-, and 2.62-fold over the vehicle-treated islets, respectively. For the long-term studies, in islets subjected to conditions mimicking a diabetic environment, GIIS was essentially preserved in MHA cultured islets, but not in TPA. Furthermore, basal (non-stimulated) insulin section, known to be increased in T2D, was reduced in MHA vs. TPA-treated islets. In all, these studies suggest that dairy-derived MHA plays a distinct role in reducing T2D risk.

Primary Faculty Mentor Name

Thomas Jetton

Secondary Mentor NetID

jkraft1

Secondary Mentor Name

Jana Kraft

Status

Undergraduate

Student College

College of Agriculture and Life Sciences

Program/Major

Biological Science

Primary Research Category

Health Sciences

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DAIRY DERIVED FATTY ACIDS IMPACT PANCREATIC BETA CELL FUNCTION

Epidemiological studies have established that full-fat dairy consumption reduces the risk of type 2 diabetes (T2D) development, particularly, the dairy-derived fatty acid trans-palmitoleic acid (16:1; TPA), although the underlying mechanisms are unknown. Recently, it has been found that 15-methyl-hexadecanoic acid (iso 17:0; MHA) may also be responsible for these effects. Since the insulin-secreting pancreatic beta cell is dysfunctional in T2D, the goal of this project was to evaluate whether TPA and MHA directly impact glucose induced insulin secretion (GIIS) in an in vitro model. The objectives of this study were to 1) determine the extent to which GIIS is influenced following short-term exposure to MHA or TPA as compared to palmitic acid (PA, a control fatty acid (FA)) in normal cultured rat pancreatic islets (microscopic structures comprised mostly of beta cells), and 2) determine the extent to which GIIS is impacted by long-term exposure to MHA or TPA in culture conditions mimicking a T2D environment. Whereas TPA, MHA, and PA short-term incubated islets in the presence of basal glucose had no significant effect on GIIS, in the presence of high glucose, GIIS was augmented 1.72-, 1.24-, and 2.62-fold over the vehicle-treated islets, respectively. For the long-term studies, in islets subjected to conditions mimicking a diabetic environment, GIIS was essentially preserved in MHA cultured islets, but not in TPA. Furthermore, basal (non-stimulated) insulin section, known to be increased in T2D, was reduced in MHA vs. TPA-treated islets. In all, these studies suggest that dairy-derived MHA plays a distinct role in reducing T2D risk.