Actually, Ramona, when excess protein is turned into glucose via gluconeogenesis, it does not cause a rise in insulin.

[the following copied from Orion1 at Protein Power BB]

Whenever the blood glucose level drops, signals are sent to put the gluconeogenetic machinery to work. This process is under the control of glucagon, cortisol or epinephrine, the three of them acting under different circumstances. Glucagon and insulin don’t work both at the same time. That is, if glucagon is “on” and controlling gluconeogenesis, insulin is “off”, and vice versa. Following this reasoning, if insulin is off (actually that means not present in excess), fat storage is also controlled, and fat release from the fat cells is favored (another process influenced by glucagon).

The process of gaining weight by storing fat into the fat cells needs fat, on one side, and insulin on the other side to activate the process. The process of gaining weight by making fat requires excess carbohydrates on one side and insulin on the other side to activate fat synthesis. With glucagon being released instead, a signal of low carbohydrate, these processes are inhibited. Thus, the mere conversion of amino acids into glucose by gluconeogenesis should not be misunderstood as a mechanism through which fat can be synthesized or deposited into the fat cells. The glucose produced by gluconeogenesis has a “tag” on it, if you will, and it will serve as a supply for blood glucose when the levels fall.

Nat