Sentences with phrase «fat cell receptors»

Blood flow, fat cell receptors, hormones and calorie intake / output all affect your ability to obliterate your love handles.

In the case of stubborn fat its slowness is related to fat cell receptors.

It increases both basal metabolic rate and lipolysis, inhibits the activity of certain fat cell receptors that prevent fat mobilization, and increases the thermic effect of food (the «energy cost» of metabolizing food).

Alpha - receptors are a type of fat cell receptor that regulates Lipolysis, the breakdown of fat.

Not exact matches

It just so happens that fat cells have human growth hormone receptors, and growth hormone stimulates them to break down triglycerides and suppresses their ability to take up and accumulate circulating lipids.

These protein and fat sources are extraordinarily critical for rebuilding healthy cell membranes with normalized insulin receptor activity.

Previous studies have found that brown fat can be coaxed into action by activating the β3 - adrenergic receptor, which is expressed on the surfaces of brown and white fat cells, as well as on cells of the urinary bladder and other tissues.

He determined that epithelial cells lining the brain's blood vessel walls contain a surface protein, or receptor, that can snag insulin, the hormone essential for metabolizing carbohydrates and fats.

In the new work, Evans» group focused on estrogen - related receptor gamma (ERRγ), a gene that is active at high levels in brown fat cells.

A potential adrenalinelike drug for weight control must target only the fat - cell receptors to avoid dangerous side effects in the cardiovascular system.

They added the modified adrenaline compound, called CP - 331679, to cultured human fat cells, and saw that the receptors were activated and were triggering a biochemical cascade inside the cell.

The bile acids accumulate in the blood and interact with the TGR5 receptor on white fat cells to change their metabolic function.

The study shows that activating the bile acid receptor TGR5 with molecules that mimic the action of bile acids (so called «mimetics») induces a remodeling of white fat cells into beige fat cells.

In research published in December 2013, the investigators found that high levels of IKK - ε and TBK1 meant that certain receptors in the fat cells of obese mice were unable to respond to neurotransmitters called catecholamines, which are generated by the sympathetic nervous system and promote «fat - burning.»

Using newly discovered information, the researchers made significant advances in developing a family of drug candidates that target a receptor known as peroxisome proliferator - activated receptors gamma (PPARγ), a key regulator of stem cells controlling bone formation and bone resorption and a master regulator of fat.

Recently, however, ephrins and Eph receptors have also been found in extracellular vesicles / exosomes — small droplets of fat released by cells, used as transport vehicles, signal transmitters or for eliminating cell components.

Deleting p75 NTR only from fat cells resulted in similar outcomes as deleting the receptors from all cell types in the body.

The researchers posit the explanation that kynurenic acid activated the cell receptor GPR35, which is found in both fat cells and immune cells.

The researchers observed that there is a particularly high number of receptors in brown fat cells which bind to the Gq protein.

The scientists discovered that the receptor helped regulate metabolic processes that control body weight, and reducing the number of p75 NTR in fat cells prevented weight gain in mice.

Originally, however, they were not examining brown fat thermogenesis, but instead were looking for clues to the function of ERRβ, a protein about which little was known at the time, except that it was closely related to ERRα, appeared in brown fat cells, and also worked as a so - called nuclear receptor — a molecular switch for gene activation that can be turned on by small lipophilic molecules or a signaling protein partner.

Infants with more methylation of a gene known as retinoid X receptor - α (RXRα), which codes for a protein involved in the development of fat cells and fat metabolism, were more likely to be obese at age 9.

The team says that this is a result of the oil triggering receptors in the digestive tract, activating the sympathetic nervous system and converting white fat cells into the beige variety.

Insulin has the capacity to bind with the receptors on muscle cells and fat cells and the enable the glucose to pass inside the cells where it's burned and used by the cells as energy source.

In addition, the chronic elevation of cortisol levels caused by excessive stress negatively affects the receptors for both insulin and leptin, which makes it harder for the body to read the signals of those hormones, thus keeping fat trapped in the cells and making you hungry all the time.

Studies show that yohimbine can accelerate fat loss by blocking the activity of alpha - receptors in fat cells.

It makes the body utilise the available fat stores by blocking the alpha receptor activity in the fat cells.

Inflammation dulls the brain's leptin receptor sites causing the body to produce more leptin to, in effect, scream at the brain to pick up what the fat cells are throwing down.

The more Insulin - resistant, meaning the more Insulin you need to make that receptor site happy to pull that Glucose in, typically the less active you are, the more fat cells you have so, the more your body will store that and not burn it.

Heat (part of the waves of the electromagnetic spectrum - radiation) does NOT tell us ANYTHING about how lipids behave, how chemical receptors behave, how fat cells hoard and become dysregulated NOR does heat EVER turn into MATTER, FAT TISSfat cells hoard and become dysregulated NOR does heat EVER turn into MATTER, FAT TISSFAT TISSUE.

When people talk about being more Insulin sensitive, that means you need less Insulin to fit into the receptor site to pull that Glucose into the cell to utilize it for fuel or store as fat — one of the two, right?

It just so happens that fat cells have human growth hormone receptors, and growth hormone stimulates them to break down triglycerides and suppresses their ability to take up and accumulate circulating lipids.

When trans fats are incorporated into cell membranes, they inhibit a wide range of biochemical reactions, such as enzymes and receptors.36

For example, carbohydrates are necessary for proper thyroid activity (specifically conversion of T3 to T4), and also because high concentration of free fatty acids can actually inhibit proper thyroid binding to it's cell receptor, a very high fat diet that excessively restricts carbohydrates lowers metabolism and causes weight gain by inhibiting thyroid activity.

Since animal protein and saturated fat or inexorably linked maybe it's the saturated fat that causes the insulin spike by blocking the insulin receptor sites in the cells

Fat cells in the belly have four times more cortisol receptors compared to fat cells located in other parts of our boFat cells in the belly have four times more cortisol receptors compared to fat cells located in other parts of our bofat cells located in other parts of our body.

This makes sense, since we do know that fat cells contain IGF - 1 receptors, and this means that IGF - 1 can interact with fat cells.

These fats compete for the same receptor sites in the cells.

Fat cells have insulin receptors.

These receptors increase the breakdown of fat, and also increase blood flow to fat cells.

Problem is that certain amino acids and fats cause fat to enter the cell and disrupt the ability of the cell to make insulin receptors.

It's better to treat the cause, not the symptom — that being too much intramyocellular fat which prevents the insulin from connecting up to the cell's receptor, enabling the cell to use the broken down starch.

Excess fat secretes too much leptin, bombarding leptin receptors on cells.

This overloads the receptors in the brain and on the fat cells themselves.

Each of your fat cells has its own growth hormone receptor.

These «fat cells» already have receptors for GH.

Cinnamon may actually stimulate insulin receptors on fat cells in the same way that insulin does, allowing excess sugar to move out of the blood and into the cells.

Leptin is secreted by fat cells and is received by receptors in the hypothalamus.

(from plants), attach to the same receptors on our fat cells that insulin attaches to.

Here's where this gets very interesting: lectins (from plants), attach to the same receptors on our fat cells that insulin attaches to.