XXXX as an Early Symptom of the AMIS Syndrome.

@entity407 @entity101 @entity28 @entity1007 @entity1560 @entity5710 @entity6 @entity2690 @entity969 @entity3190 @entity299 @entity209 @entity4854
We review evidence that the AMIS (Absence of Meal-induced @entity2690 Sensitization) syndrome describes a paradigm fundamental to development of @entity28 . The hypoglycemic response to a pulse of @entity2690 is doubled after a meal as a result of Hepatic @entity2690 Sensitizing Substance (HISS), released from the liver to act selectively on muscle, heart and kidney. In the absence of HISS action, the hypoglycemic response to @entity2690 is the same as in the fasted state, and only half of what it should be. Postprandial @entity4854 ensues, with @entity3190 , resultant @entity407 and elevated free radical stress. Storage of nutrient energy shifts from glycogen in muscle to fat. Chronic AMIS results in adiposity, occurs with age, is accelerated with @entity969 supplement, and prevented by a synergistic antioxidant. Exercise reverses AMIS, as do pharmaceuticals that mimic the "feeding signals". The AMIS syndrome develops as a sequence of pathologies based on the consequences of absence of HISS action, including adiposity as the earliest symptom. @entity299 , @entity101 , @entity1007 , and @entity1560 are related to lack of HISS action. The AMIS syndrome hypothesis is mechanistic-based and accounts for the major pathologies associated with @entity5710 , @entity28 , @entity6 and @entity209 . AMIS can be diagnosed, prevented and treated.
