Sentences with phrase «fat gene in mice»

Not exact matches

When the group stopped the gene working in mice, the animals no longer developed diabetes if fed a high - fat diet.

By combining each mouse's genome, phenome, proteome and metabolome, the scientists were able to identify a particular gene, located on their chromosome 2, and whose presence plays an important role in the development of type 2 diabetes «The mice with a high - fat diet are more or less likely to develop diabetes depending on whether this gene is active or not,» said Evan Williams, LISP PhD student and the article's co-first author.

They started with pairs of fat yellow mice known to scientists as agouti mice, so called because they carry a particular gene — the agouti gene — that in addition to making the rodents ravenous and yellow renders them prone to cancer and diabetes.

And by studying mice lacking the gene for ERRγ (and therefore unable to make the ERRy molecule), the team observed that all brown fat cells resembled white cells in these mice.

Knocking out a particular gene in muscle lets mice run twice as far as normal; knocking out the same gene in fat cells allows the animals to put on weight without developing type - 2 diabetes.

Lazar, co-first author Matthew Emmett, an MD / PhD student in his lab, and their IDOM colleagues found that mice lacking HDAC3 in their brown fat were unable to turn on the UCP1 gene and were just as susceptible to the deleterious effects of cold as mice that did not have the gene.

A single gene appears to play a crucial role in coordinating the immune system and metabolism, and deleting the gene in mice reduces body fat and extends lifespan, according to new research by scientists at the Jean Mayer USDA Human Nutrition Research Center (USDA HNRCA) on Aging at Tufts University and Yale University School of Medicine.

In mice that gorged and then fasted, the researchers saw elevations in inflammation, higher activation of genes that promote storage of fatty molecules and plumper fat cells — especially in the abdominal area — compared to the mice that nibbled all daIn mice that gorged and then fasted, the researchers saw elevations in inflammation, higher activation of genes that promote storage of fatty molecules and plumper fat cells — especially in the abdominal area — compared to the mice that nibbled all dain inflammation, higher activation of genes that promote storage of fatty molecules and plumper fat cells — especially in the abdominal area — compared to the mice that nibbled all dain the abdominal area — compared to the mice that nibbled all day.

«Turning off the FAT10 gene produces a variety of beneficial effects in the mice, including reduced body fat, which slows down aging and extends lifespan by 20 percent.»

In 1994 scientists discovered that mice missing both copies of their leptin gene develop excessive body fat, extreme hunger, and sterility.

«Deletion of FAT10 gene reduces body fat, slows down aging in mice.»

Intrigued, Turek joined with endocrinologist Joseph Bass, also at Northwestern, to study the effects of regular and high - fat diets in normal mice and mice with a dysfunctional Clock gene.

To investigate, Akhtar deleted the gene for Rac1 in female mice; their first litter of pups survived, but they were smaller than normal — probably because the milk they received contained less fat and protein than normal.

Associate Professor Amanda Sainsbury - Salis expressed surprise at the impact of the Y6 gene deletion on mice, commenting «I find it amazing that one gene, which is expressed in the small part of the brain that controls the body clock, has such a profound impact on how much fat is stored on the body, and how much lean tissue is maintained.»

He and a colleague took samples of both visceral and subcutaneous fat from the mice and, using gene chips, identified the genes in the fat cells as well as in precursor fat cells.

In mouse studies, inhibition of this gene's protein has been shown to have anti-atherosclerotic, i.e., helps fight thickening and hardening with fat on the inside of arteries and anti-diabetic effects.

Among the 20,000 mouse genes, the researchers found 200 that were different in the two fat depots.

This gene therapy resulted in high - fat diet mice having a reduced body weight, building up less fat, expending more energy, and showing evidence of improved leptin - signalling.

In other research, a knockout of the gene that encodes one type of lncRNA in mice conferred some resistance to obesity caused by a high - fat dieIn other research, a knockout of the gene that encodes one type of lncRNA in mice conferred some resistance to obesity caused by a high - fat diein mice conferred some resistance to obesity caused by a high - fat diet.

Working in mice that were put on high - fat diets to model diabetes, «we demonstrated that obesity increases the expression of pro-inflammatory genes in abdominal fat, but not in other organs such as the liver or muscle, nor in subcutaneous fat,» says Jongsoon Lee, PhD, Assistant Investigator in Joslin's Section on Pathophysiology and Molecular Pharmacology and Assistant Professor of Medicine at Harvard Medical School.

Aiming ultimately to make healthier beef, eggs, and other farm products, scientists have used a worm gene to genetically engineer mice whose tissues are unusually rich in the heart - healthy fats found mainly in fish.

With an eye toward shifting that balance, the scientists inserted into mice a gene called fat - 1, which in nematode worms produces an enzyme that converts omega - 6 fats into omega - 3 fats.

The study showed that mice lacking the SNRK gene had a significantly higher concentration of macrophages in white fat tissue compared with normal mice.

In addition, mouse brown fat in the collar bone is morphologically similar to human brown fat in the same location, produces compounds involved in the production of heat and expresses genes similar to those expressed by human brown fat.&raquIn addition, mouse brown fat in the collar bone is morphologically similar to human brown fat in the same location, produces compounds involved in the production of heat and expresses genes similar to those expressed by human brown fat.&raquin the collar bone is morphologically similar to human brown fat in the same location, produces compounds involved in the production of heat and expresses genes similar to those expressed by human brown fat.&raquin the same location, produces compounds involved in the production of heat and expresses genes similar to those expressed by human brown fat.&raquin the production of heat and expresses genes similar to those expressed by human brown fat.»

For this new study, the researchers bred mice that lack the gene for producing SNRK in fat cells.

Many of the 19 mutations were in genes that affect how mice metabolize fats and carbohydrates from food.

A gene screen revealed a number of genetic changes in the first (daughter) and third (great granddaughter) high - fat mice generations, including several linked to increased breast cancer in women, increased resistance to treatment, poor prognosis, and impaired anticancer immunity.

In mice, PGC - 1α is required for the expression of several mitochondrial genes in the liver, skeletal muscle, heart, brain, and brown faIn mice, PGC - 1α is required for the expression of several mitochondrial genes in the liver, skeletal muscle, heart, brain, and brown fain the liver, skeletal muscle, heart, brain, and brown fat.

Furthermore, after genetic analysis of the bacteria's metabolism, they discovered that genes responsible for fat synthesis had greater levels of activity in the treated mice.

In the initial report, mice harboring a mutation in the core circadian gene Clock (termed Clock mutant mice) were fed a high - fat (HF) diet and observed to develop obesity at a young age, as well as a variety of metabolic and endocrine abnormalities consistent with the metabolic syndrome (2In the initial report, mice harboring a mutation in the core circadian gene Clock (termed Clock mutant mice) were fed a high - fat (HF) diet and observed to develop obesity at a young age, as well as a variety of metabolic and endocrine abnormalities consistent with the metabolic syndrome (2in the core circadian gene Clock (termed Clock mutant mice) were fed a high - fat (HF) diet and observed to develop obesity at a young age, as well as a variety of metabolic and endocrine abnormalities consistent with the metabolic syndrome (2).

The reason for this response, Gordon says, was twofold: Firmicutes bacteria transplanted from the fat mice produced more of the enzymes that helped the animals extract more energy from their food, and the bacteria also manipulated the genes of the normal mice in ways that triggered the storage of fat rather than its breakdown for energy.