Protective effect of metformin against walker 256 tumor growth is not dependent on metabolism improvement.

Background/aims: The objective of the current work was to test the effect of metformin on the tumor growth in rats with metabolic syndrome.

Methods: We obtained pre-diabetic hyperinsulinemic rats by neonatal treatment with monosodium L-glutamate (MSG), which were chronically treated every day, from weaning to 100 day old, with dose of metformin (250 mg/kg body weight). After the end of metformin treatment, the control and MSG rats, treated or untreated with metformin, were grafted with Walker 256 carcinoma cells.

Vagus nerve contributes to metabolic syndrome in high-fat diet-fed young and adult rats.

What is the central question of this study? Different nerve contributes periods of life are known for their differential sensitivity to interventions, and increased parasympathetic activity affects the development and maintenance of obesity. Thus, we evaluated the involvement of the vagus nerve by performing a vagotomy in young or adult rats that were offered an obesogenic high-fat diet. What is the main finding and its importance? Although the accumulation of adipose tissue decreased in both younger and older groups, the younger rats showed a greater response to the effects of vagotomy in general.

Insulin oversecretion in MSG-obese rats is related to alterations in cholinergic muscarinic receptor subtypes in pancreatic islets.

Background/aims: Impaired pancreatic beta cell function and insulin secretion/action are a link between obesity and type 2 diabetes, which are worldwide public health burdens. We aimed to characterize the muscarinic acetylcholine receptor (mAChR) M1-M4 subtypes in isolated pancreatic islets from pre-diabetic obese rats that had been treated neonatally with monosodium L-glutamate (MSG).

Methods: At 90 days of age, both the MSG and the control groups underwent biometric and biochemical evaluation.

Low-protein diet in adult male rats has long-term effects on metabolism.

Nutritional insults during developmental plasticity have been linked with metabolic diseases such as diabetes in adulthood. We aimed to investigate whether a low-protein (LP) diet at the beginning of adulthood is able to program metabolic disruptions in rats. While control rats ate a normal-protein (23%; NP group) diet, treated rats were fed a LP (4%; LP group) diet from 60 to 90 days of age, after which an NP diet was supplied until they were 150 days old.

Anesthetic-induced transient hyperglycemia and insulin resistance do not depend on the sympathoadrenal axis.

Aim: Glucose homeostasis is maintained under strict physiological control in which the central nervous system is very important. Ketamine/xylazine mixture induces hyperglycemia, although the mechanism involved is unknown. We aimed to study the role of sympathoadrenal axis on glycemia and insulinemia in adult rats.