Sentences with phrase «obese mice by»

Soluble dietary fiber improves energy homeostasis in obese mice by remodeling the gut microbiota — Haiyuan Wang — Biochemical and Biophysical Research Communications

The researchers were also able to turn normal - birthweight pups into obese mice by injecting extra leptin 5 to 10 days after birth.

Not exact matches

Scientists reached this conclusion by transferring microbes from bypass - treated obese mice to a group of lean mice raised in sterile conditions that left them with no intestinal bacteria at all.

«We did not do it using a genetic strain of obese mice, but mice that became obese the way that people do, by eating a high - fat, high - sugar diet.»

Moreover, obese - phenotype mice were invaded by members of the Bacteroidales from the lean mice, but, happily, the lean animals resisted invasion by the obese microbiota.

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.»

By comparing the behavior of XBP - 1s in the obese mice with that in lean, healthy ones, he discovered an inflammatory protein that modifies XBP - 1s in healthy animals so it can be shuttled into the nucleus.

New study shows that in obese mice a hormone secreted by fat cells goes undetected and the regulation of appetite is thrown off; findings could trigger treatment

When the Cornell team cultured human breast cancer cells on matrix deposited by fat - derived cells from obese mice, the cancer cells grew faster than they did on the matrix of cells from slimmer mice.

Now Catherine Suter at Victor Chang Cardiac Research Institute in Sydney and her colleagues have investigated the longer - term effects of paternal obesity by mating obese male mice with lean females.

To explore that question, a team led by Cornell University biomedical engineer Claudia Fischbach first showed that female mice that were obese, because of genetics or a high - fat diet, had more fibrous mammary fat pads with straighter collagen fibers than those seen in lean mice (see image).

Kravitz has a background in studying Parkinson's disease, and when he began conducting obesity research a few years ago, he was struck by similarities in behavior between obese mice and Parkinsonian mice.

«TXN is especially potent in reducing insulin resistance in mice made obese by feeding a high - fat diet,» said Cristobal Miranda, an associate professor at the Linus Pauling Institute who was involved in the research.

This difference may be explained by the reduced levels of normal CST in obese mice compared to the lean control animals.

The researchers tested their theory by orally administering a drug that inhibits DNA - PK and found that, in addition to preventing weight gain in the mice, the inhibitor drug boosted mitochondrial content in skeletal muscle, increased aerobic fitness in obese and middle aged mice, and reduced the incidence of obesity and type - 2 diabetes.

As a result, these researchers found that one strain of mice which were genetically prone to become obese became resistant to excess weight gain after their populations of gut microbiota were transformed simply by an sharing an environment with other mice.

The results of this initial study, and the description of the use of these two diets are presented in the paper by (4) Van Heek et al (1997), «Diet induced obese mice develop peripheral, but not central resistance to leptin».

(17) Slow - aging growth hormone receptor knockout (GHRKO) mice are obese, but highly insulin sensitive: in such animals, surgical removal of visceral adipose tissue impairs insulin secretion and peripheral insulin action, in part by reducing adiponectin production.

Interestingly, it has been reported that mice with a mutation in Kap1 were obese and had behavioral problems, and the lower expression of Kap1 that we have found in the blastocysts produced by IVC could also be related to the behavior problem reported in mice generated by IVC [43].

In 1994, it was discovered that a protein hormone called leptin, which is released from fat cells and monitored by the brain, was deficient in a certain strain of genetically mutated obese mice.

This idea is supported by animal studies, showing that mice without any bacteria in their intestines had lower amounts of body fat, and did not become obese or insulin resistant when put on a high - fat diet.

In rodents, ketogenic diets reduce reactive oxygen species in the brain34 and reduce central inflammation and reactive oxygen species in a model of multiple sclerosis.35 Two clinical papers have found that ketogenic diet feeding of 12 weeks to 6 months reduced signs of liver inflammation in obese patients with nonalcoholic fatty liver disease (in addition to improving various other physiological and biochemical variables).36, 37 Unfortunately, basic research into non-alcoholic fatty liver disease has been hampered by species differences between mice and humans in their hepatic reaction to ketogenic diets.38

Because obesity is known to increase a woman's risk of endometrial cancer by 200 percent, a team of researchers led by oncologist Leena Hilakivi - Clarke of Georgetown Lombardi Comprehensive Cancer Center in Washington, D.C., decided to examine the development of endometrial cancer in obese mice to that in non-obese mice.

Calorie Restriction - like Effects of 30 Days of Resveratrol Supplementation on Energy Metabolism and Metabolic Profile in Obese Humans Cell Metabolism 2011 (Nov 2); 14 (5): 612 — 622 ~ FULL TEXT The result of just 30 days on resveratrol were impressive: (1) The same gene regulators (AMPK, SIRT1 and PGC - 1a) were activated in this study as are activated by caloric restriction and resveratrol in mice and endurance training in humans.

This study has examined the effect of alpha - lipoic acid on glucose uptake by cultured L6 muscle cells and different types of skeletal muscles in normal lean (+ / +) and severely insulin - resistant, obese - diabetic (ob / ob) mice.

Citing studies of female mice where those who were obese before and during pregnancy had heavier children, there is evidence that rather than changing the DNA itself the toll is exacted by affecting the switches that control which genes are switched on and switched off.