The effects of diet induced changes of Kir4.1 function in astrocytes and the modulation of homeostatic mechanisms of the regulation of food intake.


Violet Witchel

Document Type


Publication Date

Summer 2017

JAX Location

In: Student Reports, Summer 2017, Jackson Laboratory


Jackson Laboratory was one of the first to clearly demonstrate that an obesogenic diet rapidly changes the excitability of AgRp neurons, causing a negative feedback loop reinforcing the obese state and promoting an excess energy imbalance. However it remains unclear which mechanism(s) diet composition uses to increase neuronal excitability. We hypothesize that diet-induced changes in Kir4.1 function in astrocytes modulate the activity of AgRP neurons and disrupt homeostatic mechanisms in the regulation of food intake. This Study looks at the significance of diet induced changes in the function of Kir4.1 in astrocytes and the control of homeostatic mechanisms and the regulation of food intake. To research this we used either genetically obese Ob/Ob mice fed either a low-fat rodent chow or a high-fat diet as well as wild type C57Bl6/J fasted overnight, fasted overnight and refed, 2 day HFD, or chow diets and analysed the effects of those diets on Kir4.1 expression, astrocyte reactivity, and microglia using confocal fluorescence microscopy. We assessed the levels of fluorescence using FIJI and determined that a HFD does not have a significant effect on homeostatic mechanisms in wild type mice, however in OB and DIO mice it is shown to reduce the presence of markers for Iba l , GFAP, and Kir4.1

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