Insulin is defiantly a satiety hormone my friend. Potatoes (one of the most insulinogenic foods known to man) is also the most satiating food! And insulin is required for leptin synthesis.
What causes leptin-resistance is the same as what causes insulin-resistance; high levels of FFAs and triglycerides which inhibit the transport of leptin thru the blood-brain-barrier. If you were starving to death, your subcutaneous body-fat stores are becoming depleted and the levels of FFAs in the blood are increasing. This scenario would cause leptin-resistance to occur in order to make you hungry, so that you eat and stop starving to death. The decrease in insulin-secretion and the depletion of subcutaneous body-fat reservoirs decreases the amount of leptin your adipocytes make, plus the high levels of FFAs and triglycerides circulating in the blood then impairs the leptin that is already present within the body from promoting its satiating effects.
Eating starches and sugars and spiking your insulin, lowers FFAs and shuttles fat inside the adipocyte, which enables leptin-synthesis to occur and enables leptin to make its way inside to brain and decrease appetite. Rule of thumb: anytime the adipose-tissue is undergoing lipolysis (like in starvation or diabetes) leptin-signaling decreases.
Diabetics have reduced androgens and IGF-1 because they either can't make enough insulin to stimulate IGF-1 and testosterone production... or the insulin they do make is unable to stimulate IGF-1 and testosterone production due to the body being resistant to the effects of insulin.
Atkins and other high-fat ketogenic-diets mimic the effects of type-1 diabetes. One of the consequences of diabetes is an increase in ketones and FFAs and also accelerated weight-loss (as in wasting away; depletion of subcutaneous-fat reserves and a decrease in muscle-mass due to excessive lipolysis and proteolysis).
Edited by misterE, 31 May 2014 - 04:01 AM.