Fructose is a simple sugar found in fruit and honey, but it is also used as sweeteners via added sugars, syrups, or high fructose corn syrup in processed foods or beverages. This is a concern because excessive fructose intake is linked to obesity and its comorbid diseases like diabetes and cardiovascular disease. We show that mice consuming a high fructose diet eat more and gain more weight and body fat than mice consuming chow or a high glucose diet. As the brain is a vital organ mediating the actions of fructose, we determined the neuronal maladaptations underlying fructose-mediated obesity. Interestingly, fructose feeding increased excitatory drive to hypothalamic neurons known to stimulate food intake, and this excitatory drive is comparable to that seen during hunger. This presentation will examine the synaptic plasticity and whether it may be reversed with the cessation of fructose feeding. Our findings indicate that central maladaptations following excessive fructose consumption may contribute to overeating and the development of diet-induced obesity.
The F.C. MacIntosh Lectureship supports special seminars in honour of Dr. F.C. MacIntosh.