Healthy Subjects Clinical Trial
Official title:
The Role of IntraNasal Insulin in Regulating HepaTic Lipid COntent in HUMANS a Randomized, Controlled, Double Blinded Trial
Non-alcoholic fatty liver disease (NAFLD) is a common human liver pathology, closely
associated with the obesity pandemic and insulin resistance. In the insulin resistant state
the liver remains sensitive to pro-lipogenic signals of insulin, which further promote lipid
accumulation. Secretion of very-low-density-lipoproteins (VLDL), the main carriers of
triglycerides (TG) in the plasma, is the principal pathway for the liver to mobilize and
dispose of lipids. Thus, hepatic TG export must not be too low in order to prevent steatosis.
Our preliminary data from animal experiments suggest that enhanced brain insulin signaling
promotes hepatic VLDL secretion, and reduces lipid accumulation in the liver. It remains to
be tested whether other insulin sensitive tissues, such as the myocardium or the skeletal
muscle, are also affected. In humans, neuropeptides, including insulin, can be delivered to
the brain via an intranasal (IN) route of administration, without causing relevant systemic
side effects.
Therefore, we hypothesize that by enhancing brain insulin signaling using chronic IN insulin
administration hepatic TG export increases and prohibits lipid accumulation in the liver and
other insulin sensitive tissues, such as the myocardium and the skeletal muscle.
n/a
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