Block 3 Lecture 36 Flashcards
what is the initial phase of hyperinsulinemia called
compensatory hyperinsulinemia
what is the second stage of hyperinsulinemia called
relative beta cell failure
what inhibits lipolysis
insulin
what is the result of the inhibitory action of insulin on lipolysis being reduced?
there will be an increased production of FFAs
what does an increase in plasma FFAs do
it will lead to an increase in insulin secretion from beta cells, due to enhanced mitochondrial oxidation of FFAs leading to increased ATP synthesis and then to enhanced insulin secretion
what marks the phase change from compensatory hyperinsulinemia to relative beta cell failure
the peak in insulin levels from increased lipolysis
what can contribute to relative Beta cell failure
oxidative stress and apoptosis of B-cells
what are elevations of ROS in B-cells associated with
mitochondrial dysfunctions which would decrease ATP producing capacity of the cell and decreased secretion of insulin
what inhibits gene transcription
FFAs, TNF alpha, and resistin
what can the loss of beta cells be contributed to
oxidative stress, long term glucose intolerance, and elevated FFAs
what has leptin been linked with
pro-inflammatory activity in the Beta cell, Beta cell apoptosis, and decrease in beta cell mass
what does apoptosis involve the activation of
intracellular enzymes called caspases
what are caspases
cysteine proteases critical to programmed cell death
what do sulfonylureas do
enhance glucose stimulated insulin secretion in remaining B cells in individuals with metabolic syndrome and type 2 diabetes
what is the sulfonylurea mechanism
they bind to the Katp, close them and cause membrane depolarization causing Ca2+ channels to open and secrete insulin
