On 2017 Jul 27, Richard Sauerheber commented:

(from the author) Many have argued that insulin stimulates glucose transport in sensitive cells by recruiting already pre-synthesized glucose transport molecules that are inside the cell waiting to be inserted after insulin binds to cell surface receptors. This however would be an energy-requiring and relatively slow process, to insert water soluble transport protein sections through the hydrophobic lipid bilayer. The function of insulin is to conserve energy after eating a meal, storing glucose for future energy needs in the form of glycogen, as well as other foodstuffs, and to quickly react to meal eating, and then to quickly deactivate energy storage between meals. So energy use, such as that required to insert transporters into an already-formed membrane would be wasteful and a contradiction in function. Also, the insulin stimulation of glucose transport is very rapid, finished within a minute, and the reverse, the deactivation of the transport rate, occurs quickly after insulin washes away, as when insulin levels are miniscule between meals. Removal of transporters from a membrane, to be stored inside the cell for later use again when the next meal is consumed, is a cumbersome notion. The data here point to a much more sophisticated and efficient design, where allosteric conformational changes can cause rapid activation and deactivation cycles in transporter activity when insulin is present and then absent, as during and then between meals throughout the day in the in vivo setting. For all the published data suggesting to investigators this is not a proper view, understand that such presented evidence is not compelling or beyond reasonable doubt, including microscopic observations of what are thought to be widespread intracellular transporters waiting for repeated, rapid re-insertion into, and re-removal from, the plasma membrane. The view described here caused my NIH grant renewal in the 1980's to be rejected. My research position eventually was terminated and I went into teaching (which I fortunately dearly love). Meanwhile, I stand by these observations and continue to teach them.

On 2017 Jul 27, Richard Sauerheber commented:

(from the author) Many have argued that insulin stimulates glucose transport in sensitive cells by recruiting already pre-synthesized glucose transport molecules that are inside the cell waiting to be inserted after insulin binds to cell surface receptors. This however would be an energy-requiring and relatively slow process, to insert water soluble transport protein sections through the hydrophobic lipid bilayer. The function of insulin is to conserve energy after eating a meal, storing glucose for future energy needs in the form of glycogen, as well as other foodstuffs, and to quickly react to meal eating, and then to quickly deactivate energy storage between meals. So energy use, such as that required to insert transporters into an already-formed membrane would be wasteful and a contradiction in function. Also, the insulin stimulation of glucose transport is very rapid, finished within a minute, and the reverse, the deactivation of the transport rate, occurs quickly after insulin washes away, as when insulin levels are miniscule between meals. Removal of transporters from a membrane, to be stored inside the cell for later use again when the next meal is consumed, is a cumbersome notion. The data here point to a much more sophisticated and efficient design, where allosteric conformational changes can cause rapid activation and deactivation cycles in transporter activity when insulin is present and then absent, as during and then between meals throughout the day in the in vivo setting. For all the published data suggesting to investigators this is not a proper view, understand that such presented evidence is not compelling or beyond reasonable doubt, including microscopic observations of what are thought to be widespread intracellular transporters waiting for repeated, rapid re-insertion into, and re-removal from, the plasma membrane. The view described here caused my NIH grant renewal in the 1980's to be rejected. My research position eventually was terminated and I went into teaching (which I fortunately dearly love). Meanwhile, I stand by these observations and continue to teach them.