When insulin is deficient , GLUT4 transporters are not inserted into the cell membranes , glucose is not transported into the cells and the blood glucose concentration increases.
Insulin deficiency provides more amino acid and glycerol substrates for glucose synthesis ie increased gluconeogenesis .
With a deficiency of insulin, there is both increased hepatic glucose production through increased glycogenolysis and gluconeogenesis as well as decreased glucose use. The result is hyperglycemia.
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A diverse range of clinical syndromes with a shared anatomic location inside the basal ganglia are known as basal ganglia disorders.
<h3>What is functional anatomy of basal ganglia disorders model ?</h3>
A model in which particular types of basal ganglia disorders are associated with changes in the function of subpopulations of striatal projection neurons. This model aims to explain the variety of clinical manifestations associated with insults to various parts of the basal ganglia.
- This model is based on an analysis of post-mortem anatomical and neurochemical data from humans and experimental animals. The excess of aberrant movements that characterise hyperkinetic diseases are thought to be caused by a specific dysfunction of striatal neurons that project to the lateral globus pallidus.
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