In animal studies, the whole-body glucose disposal effect of insulin is low in the fasted state
or after atropine infusion, but doubles after a meal, consistent with the hepatic insulin …

The hypotheses were: HISS-dependent insulin resistance (HDIR) accounts for insulin
resistance that occurs with aging; HDIR is the initiating metabolic defect that leads …

Absence of meal-induced insulin sensitization (AMIS) results in a predictable progression of
dysfunctions, including postprandial hyperglycemia, compensatory hyperinsulinemia …

Different diets have distinct impacts on glucose homoeostasis, for which insulin sensitivity
(IS) after a meal (postprandial IS) is highly relevant. Postprandial IS depends upon hepatic …

The dynamic response to insulin is highly potentiated after meal ingestion, and this meal-
induced insulin sensitization (MIS) in healthy subjects is dependent on cholinergic …

We have previously demonstrated that progressive development of absence of meal-
induced insulin sensitization (AMIS) leads to postprandial hyperglycemia, compensatory …

A series of in vivo and in vitro studies using animal and human models in the past 15 years
have demonstrated that approximately 55%(~ 66% in humans) of the glucose disposal effect …

Hepatalin is a hormone secreted by the liver in response to pulses of insulin after a mixed
nutrient meal, but only if the liver receives two permissive synergistic feeding signals from …

Meal-induced insulin sensitization (MIS) describes the augmented postprandial response to
insulin through action of the hepatic insulin sensitizing substance (HISS). HISS-action is …

We review evidence that the AMIS (Absence of Meal-induced Insulin Sensitization)
syndrome describes a paradigm fundamental to development of obesity. The hypoglycemic …