Insulin oscillation the oscillations become synchronized by electrical coupling between closely located beta cells that are connected by gap junctions, and the periodicity is more uniform (3-6 min). Pulsatile insulin release from the entire pancreas requires that secretion is synchronized between 1 million islets within a 25 cm long organ. Much like the cardiac pacemaker, the pancreas is connected to cranial nerve 10, and others, but the oscillations are accomplished by intrapancreatic neurons and do not require neural input from the brain. It is not entirely clear which neural factors account for this synchronization but ATP as well as the gasses NO
Insulin resistance with insulin resistance. It is hypothesized that increasing cell membrane fluidity by increasing PUFA concentration might result in an enhanced number of insulin receptors, an increased affinity of insulin to its receptors, and a reduced insulin resistance, and vice versa. Many stressing factors may lead to increased cortisol in the bloodstream. Cortisol counteracts insulin, contributes to hyperglycemia-causing hepatic gluconeogenesis, and inhibits the peripheral utilization of glucose, which eventually leads to insulin resistance. It does this by decreasing the translocation of glucose transporters (especially GLUT4) to the cell membrane. Inflammation by itself also seems to be implicated in causing insulin resistance.