Sentences with phrase «insulin stimulation»

"Insulin stimulation" refers to the process of increasing the production or release of insulin in the body. Insulin is a hormone that helps regulate blood sugar levels. So, when someone says "insulin stimulation," they mean promoting the body to produce more insulin or make it work more effectively to control blood sugar. Full definition
A0.5 values after acute insulin stimulation in the range of 0.1 pmol / l to 10 nmol / l were significantly lower compared with A0.5 at insulin concentrations of 0.1 — 1 μmol / l.
A0.5 values after acute insulin stimulation in the range of 1 pmol / l to 1 nmol / l are lower than A0.5 values at insulin concentrations of 0.1 — 1.0 μmol / l (Fig. 4B).
Acute insulin stimulation increased glucose transport by 21 % in control cultures precultured at 1 pmol / l insulin, but at higher insulin concentrations we could not detect an effect of insulin on glucose uptake.
Human satellite cell cultures were precultured for 4 days at different insulin conditions, and the fractional activity (FV0.1) of GS was determined under basal conditions and after acute insulin stimulation as described in research design and methods.
In accordance, Jackson et al. (9) showed that preculturing at 0.1 μmol / l insulin decreased the effect of acute insulin stimulation on glucose transport.
Diabetic myotubes expressed a reduced basal glucose uptake compared with control cultures when precultured at equal low - insulin concentrations, and the increase in fractional velocity of GS was reduced after acute insulin stimulation at identical glucose uptake rates in diabetic cultures precultured at low insulin concentrations.
The Hill coefficient was ∼ 1.0 for all culture conditions and did not vary with acute or chronic insulin stimulation in either control cultures or cultures established from diabetic subjects (P > 0.05, data not shown).
Protein: Dietary protein can increase insulin stimulation too, and in this case can increase fat storage as well.
Lower total and LDL - cholesterol concentrations after the EB period might be due to a lower insulin stimulation of hydroxyl methyl glutaryl - Co-A reductase.
Human satellite cell cultures were precultured for 4 days at different insulin conditions, and the glucose transport activity was determined under basal and after acute insulin stimulation as described under research design and methods.
Acute insulin stimulation increased glucose transport in type 2 cultures to corresponding values at insulin concentrations of 1 pmol / l and 1 nmol / l, but it decreased in type 2 cultures precultured at 1 μmol / l (P < 0.05).
The U-formed shape of the dose - response curve for type 2 diabetic cultures and the parallel curves for high insulin concentration in control cultures indicate that the mechanism for the primary defect is different from the mechanism responsible for the induced reduction in acute insulin stimulation of GS.
GLUT4 is translocated to the cell membrane in response to insulin stimulation and takes up glucose in blood, decreasing blood sugar levels.
Acute insulin stimulation significantly increased GS activity at 0.1 mmol / l in both diabetic (P < 0.0001) and control (P < 0.0001) cultures; however, GS activity at 10 mmol / l was unaffected by acute insulin stimulation in both culture types (P > 0.55 in diabetic and control cultures).
Taken together, our data suggest that insulin resistance in patients with type 2 diabetes contain at least two important defects: a reduced glucose transport under basal conditions and a reduced GS activity under acute insulin stimulation, implicating a reduced glucose uptake in the fasting state and a diminished insulin - mediated storage of glucose as glycogen after a meal.
Acute insulin stimulation significantly decreases A0.5 for GS in diabetic cultures precultured at 0.1 nmol / l to 0.1 μmol / l insulin, whereas higher or lower chronic insulin concentrations diminished the effect of acute insulin stimulation (Fig. 4B).
In accordance with other studies, we found an increased glucose uptake under acute insulin stimulation in cultures established from control subjects precultured under basal physiological insulin concentrations, but when precultured at a higher insulin concentration, we could not see an effect on acute insulin stimulation indicative of induced insulin resistance (10).
Human satellite cell cultures were exposed for 4 days to different insulin conditions, and the GS activity was measured at 0.1 and 10 mmol / l G6P under basal and after acute insulin stimulation (Ins.
Before determining glucose uptake, all cell cultures were exposed to basal medium for 1 h. Cultures used for acute insulin stimulation were exposed for 1 h to high insulin as described for GS assays.
Our data suggest that insulin resistance in patients with type 2 diabetes comprises at least two important defects under physiological insulin concentrations: a reduced glucose transport under basal conditions and a reduced GS activity under acute insulin stimulation, implicating a reduced glucose uptake in the fasting state and a diminished insulin - mediated storage of glucose as glycogen after a meal.
Acute insulin stimulation significantly increased the fractional activity FV0.1 of GS in control cultures in the range of 0.1 pmol / l to 0.1 nmol / l (P < 0.05) and in diabetic cultures in the range of 0.1 pmol / l to 1.0 nmol / l (P < 0.05), whereas higher insulin concentrations diminished the effect of acute insulin stimulation in a dose - dependent pattern.
Human satellite cell cultures were precultured for 4 days at different insulin conditions, and the activity constant A0.5 of GS was determined under basal and after acute insulin stimulation as described in research design and methods.
We could not find significant changes in G6P content as either a function of increasing chronic insulin concentrations or between values before and after acute insulin stimulation.
Acute insulin stimulation significantly decreases A0.5 for GS in cultures precultured at 0.1 pmol / l to 0.1 nmol / l and 10 — 100 nmol / l insulin, whereas higher chronic insulin concentrations diminished the effect of acute insulin stimulation (Fig. 4A).
The whey portion of the dairy is felt to play the larger role in insulin stimulation, but cheese may also have significant remnants of whey protein left.
a b c d e f g h i j k l m n o p q r s t u v w x y z