Hello, my name is Justine Johnson. I'm an OMS3 at the Idaho College of Osteopathic Medicine. The title of my research is Dietary Alleric Acid Induces Specific Effects on Adipokine Secretory Profiles in Visceral Adipocytes from Healthy and Type 2 Diabetes Mellitus Patients. Let's start by talking about obesity. The CDC reports that more than two in five U.S. adults have obesity, and the prevalence of obesity in 2020 was over 40%. We see many metabolic changes with obesity, including increased blood lipids that eventually cause dyslipidemia, abnormal adipokines, and inflammation. These changes can lead to other chronic diseases such as type 2 diabetes mellitus due to insulin resistance. The inflammatory adipokine leptin is increased while there is a decrease in the adiponectin and anti-inflammatory adipokine, which promotes insulin sensitivity. With obesity and type 2 diabetes reaching pandemic proportions worldwide, it is increasingly important to understand the role of environmental factors such as our diet in the pathophysiology underlying adipose tissue dysfunction. So, let's talk about different diets and specifically focus on dietary fats. The Mediterranean diet is high in DHA and omega-3 that is found in fish oil. This type of fat is anti-inflammatory compared to the Western diet, which is high in palmitate, a pro-inflammatory saturated fat derived from animals. Coconut oil, which is composed of multiple different medium chain saturated fatty acids, with the primary contributor being lauric acid, was a focus of my research. Coconut oil as a healthy dietary fat remains controversial. The reason coconut oil has been proposed as a healthier fat and potential tool for weight loss is that it is processed by the body differently than saturated fats derived from animals. These medium chain fatty acids are quickly absorbed and used directly in the body for energy without involvement in the biosynthesis or transport of cholesterol. The direct effects of lauric acid on adipose tissue at the cellular level, including adipocyte differentiation, capabilities to store fat, or their functional capacity to secrete adipokines remains poorly understood. Thus, our study aimed to investigate these effects in vitro using visceral human adipocytes and compare them to two other fatty acids, DHA and palmitic acid. Moving on to experimental design, I purchased two different cell lines of human visceral pericardial pre-adipocytes, one from a healthy donor and the other from a donor with type two diabetes mellitus. I differentiated these for two weeks into mature adipocytes. I then treated the cells with the three different fatty acids as a complex with bovine serum albumin for two different time points, four and eight days. At each of those time points, I harvested the cells and conditioned media, ran ELISAs for adiponectin and leptin from the conditioned media and did an oil red O staining. So starting with figure one on the upper left-hand corner, these are the ELISA measurements of adiponectin secretion, the anti-inflammatory adipine. The graph on the left are healthy cells while the type two diabetes cells are on the right. The orange represents lauric acid. As you can see, lauric acid decreased adiponectin secretion in both cell lines compared to the vehicle control, reaching its maximum effect at day four. This can be compared to DHA in the gray, which increased adiponectin secretion in both cell lines. Moving on to figure two to the right are the measurements of leptin between the healthy cells and type two diabetes cells. This graph shows that lauric acid up-regulated leptin secretion in healthy adipocytes while it decreased leptin secretion in type two diabetes cells, having opposing effects between the different cell lines. Let's dive deeper into this by moving on to figure three. So now we are just comparing vehicle control in the black and lauric acid in the orange on treatment day four, since this is where we observe maximum effects on the cells. In the bar graph on the left, this shows lauric acid down-regulated secretion of adiponectin in both groups with more pronounced effects in the type two diabetes cells. This is a particularly important finding since adiponectin promotes insulin sensitivity. We would want to see an increase in its secretion not a decrease as seen with lauric acid treated cells compared to the DHA treated cells. To the right in the bar graph of leptin concentration, again, comparing vehicle control and lauric acid, you can see at baseline, the type two diabetes cells already have significantly less leptin and lauric acid treatment further down-regulated leptin secretion in these cells. This suggests a pre-existing dysfunctional leptin pathway in these cells, which lauric acid further contributed to. All right, so this is the oil reto staining, which was used to visualize fat storage. The red represents lipid droplets. As you can see, there really isn't a difference between vehicle DHA and lauric acid. However, palmitic acid treated cells appear to have more fat accumulation, which we would expect to see of a saturated fat. So these are my conclusions. Lauric acid does not affect fat storage capacity of adipocytes. Lauric acid down-regulates adiponectin secretion in adipocytes with more pronounced effects on cells isolated from patients with type two diabetes. And lastly, lauric acid significantly down-regulates leptin secretion in adipocytes from patients with type two diabetes and has an opposite effect in cells from healthy subjects. So overall, the results suggest that coconut oil may have pro-inflammatory effects on adipocytes and further contribute to adipose tissue dysfunction as seen in obesity. However, additional research is needed to address the specific changes that were observed. Thank you so much for listening.

lauric acid

adipokine secretion

type 2 diabetes

adiponectin

coconut oil