A synergistic, balanced antioxidant cocktail, protects aging rats from insulin resistance and absence of meal-induced insulin sensitization (AMIS) syndrome.

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 of an i.v. injection of insulin in the fed state is dependent on the action of a second hormone, hepatic insulin sensitizing substance (HISS), which is released from the liver and stimulates glucose uptake in muscle, heart and kidneys.

Fatty Liver and Fatty Heart-Where do They Stand in the AMIS Syndrome?

Meal-induced insulin sensitization (MIS) refers to the augmented glucose uptake response to insulin following a meal. Absence of MIS (AMIS) causes significant decrease in post-meal glucose disposal leading to postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, adiposity, increased free radical stress, and a cluster of progressive metabolic, vascular, and cardiac dysfunctions referred to as the AMIS syndrome. We tested the hypothesis that fat accumulation in the liver and heart is part of the AMIS syndrome.

Interaction of antioxidants and exercise on insulin sensitivity in healthy and prediabetic rats.

Meal-induced insulin sensitization (MIS) describes the augmented postprandial response to insulin through action of the hepatic insulin sensitizing substance (HISS). HISS-action is impaired in insulin resistance associated with aging and type 2 diabetes, but could be preserved by the antioxidant cocktail SAMEC, along with voluntary exercise. In this study, we tested whether antioxidant supplementation during voluntary training would interact with the effects of exercise on HISS-mediated glucose uptake in healthy and prediabetic rats.

Lifestyle impact on meal-induced insulin sensitization in health and prediabetes: a focus on diet, antioxidants, and exercise interventions.

The augmented whole-body glucose uptake response to insulin during the postprandial state is described as meal-induced insulin sensitization (MIS). MIS occurs when the presence of food in the upper gastrointestinal tract activates 2 feeding signals (activation of hepatic parasympathetic nerves and elevation of hepatic glutathione level), and causes insulin to release hepatic insulin sensitizing substance (HISS), which stimulates glucose uptake in skeletal muscle, heart, and kidneys. HISS action results in nutrient storage, primarily as glycogen.

Exercise enhancement of hepatic insulin-sensitising substance-mediated glucose uptake in diet-induced prediabetic rats.

The sensitisation of insulin action in response to a meal (i.e. meal-induced insulin sensitisation, MIS) represents one of the major means of increased glucose disposal in peripheral tissues during the postprandial state.

Insulin sensitization by voluntary exercise in aging rats is mediated through hepatic insulin sensitizing substance (HISS).

Background: Food in the upper gastrointestinal tract potentiates the glucose uptake response to insulin. Meal-induced insulin sensitization (MIS) occurs as a result of insulin-mediated release of hepatic insulin sensitizing substance (HISS) that increases glucose uptake in peripheral tissues. HISS release decreases with age, and exercise causes metabolic improvements in aging, therefore it is important to analyze the effect of exercise on age-associated decline in HISS-action.

Anti-inflammatory, analgesic and diuretic activity of Polygonum lanatum Roxb.

The hexane (PLH), ethyl acetate (PLE) and methanol (PLM) extracts of dried whole plant parts of Polygonum lanatum Roxb. (Family, Polygonaceae) obtained by successive cold extraction, were subjected to evaluate anti-inflammatory, analgesic and diuretic activity in experimental animals. Oral administration of either PLH and PLM at a dose of 300 mg/kg body weight showed statistically significant (p < 0.