A key enzyme in cholesterol biosynthesis is 3 - hydroxy -3-methylglutaryl — CoA reductase (the target for statins), which is
activated by insulin, which means that an increase in blood glucose and consequently of insulin levels will lead to increased endogenous cholesterol synthesis.
Since GLUT - 4 is
activated by insulin, this extra efficiency will allow insulin levels to fall.
Now, Fox01 is a downstream of Akt, and if you recall, Akt can be
activated by the insulin receptor signaling.
This involves the phosphorylation event typically actually activated with PI3 kinase, which is also not only
activated by insulin, but also it can be activated by leptin.
Not exact matches
By removing an attached string of amino acids, the enzyme
activates hormones such as
insulin and two hormones that may play a role in obesity — glucagonlike peptide 1 and melanocortin - stimulating hormone.
In a healthy mother, this enzyme is
activated by hormones like
insulin and
insulin - growth factors (IGFs), kick - starting a relay race within cells which stimulates nutrient uptake and, as a result, normal growth and metabolic function.
FoxO1 acts as a sensor of blood sugar levels and responds
by activating insulin production.
Our vigorous genetic approach combined with direct observations of Dilp production in IPCs provides the first evidence, to our knowledge, that Bombesin - related receptor signaling
activated by its endogenous ligand promotes
insulin production.
This is quite a complex pathway and I don't have time to go through details, but just briefly, glucose metabolism is regulated
by insulin, so is lipid metabolism and this is one of many pathways where
insulin activates a number of kinases, but particularly Akt.
It's actually a very important transcription factor that's regulated
by insulin, and this is involved in
activating genes involved in fatty acid synthesis and so - called lipogenesis, which is synthesizing new lipids and this is, therefore, important in lipid metabolism.
Specifically, it works
by activating glucagon, which works in opposition to
insulin to keep your blood glucose levels balanced.
A sustained modest weight - loss of five to 10 % body - weight is associated with improvements in various indices of cardiometabolic health including but not limited to
insulin sensitivity, vascular function, blood pressure and lipid levels.3 These beneficial effects of weight - loss can be partially explained
by accompanying reductions in adipose tissue mass and dysfunction.5 There is however, some evidence to suggest that energy restriction (ER) alone can confer metabolic changes which are independent to those of weight - loss,
by facilitating an acute negative energy balance 6 - 9 and / or
by activating adaptive stress response pathways.10
Stimulation of beta - amyloid precursor protein trafficking
by insulin reduces intraneuronal beta - amyloid and requires mitogen -
activated protein kinase signaling.
Insulin molecules are highly vulnerable to oxidation — attack
by free radicals — and this makes them less effective at
activating glycogen stores.
Berberine improves
insulin signal transduction
by stimulating glucose intake via the activation of the AMP -
activated protein kinase pathway.
«There are multiple interactive pathways and molecular mechanisms
by which CR (calorie restriction) and IF (intermittent fasting) benefit neurons including those involving
insulin - like signaling, FoxO transcription factors, sirtuins and peroxisome proliferator -
activated receptors.
Engagement of the
Insulin - sensitive Pathway in the Stimulation of Glucose Transport
by Alpha - lipoic Acid in 3T3 - L1 Adipocytes Diabetologia 2000 (Mar); 43 (3): 294 — 303 These results indicate that R (+) alpha - lipoic acid directly
activates lipid, tyrosine and serine / threonine kinases in target cells, which could lead to the stimulation of glucose uptake induced
by this natural cofactor.
Exercise increases
insulin sensitivity and, if it's intense enough, can even
activate something called non-
insulin dependent glucose uptake, which is a method for increased glucose uptake
by the muscles without using
insulin at all.
Furthermore, available evidence from in vitro studies suggests that one of the possible mechanisms through which phthalates exposure may affect
insulin sensitivity is oxidative stress, either
by activation of peroxisome proliferator —
activated receptors (20) or
by changes in mitochondrial membranes potential and permeability (21).