Sentences with phrase «obese mice with»

Reduced adiposity and improved insulin sensitivity in obese mice with antisense suppression of 4E — BP2 expression.

Consistently, killing the intestinal bacteria of obese mice with an antibiotic treatment reduced body fat and improved insulin sensitivity (4, 5).

The final group, the obese mice with an inability to create myostatin remained fat, but they also exhibited perks of their new ability — they were much stronger than their counterparts and their heart and metabolic health had improved.

there is a 5-fold increase in number of insulin - secreting cells per islet in obese mice with high insulin secretion

In genetically programed insulin - resistant obese mice with increased appetite and reduced physical activity, targeted restoration of Pomc function only within 5 - hydroxytryptamine 2c receptor containing cells induces sex differences in energy balance (267).

Treating obese mice with CST inhibited the recruitment of monocyte - derived macrophages to the liver and decreased inflammation, suggesting CST is an anti-inflammatory peptide.

Treating obese mice with catestatin (CST), a peptide naturally occurring in the body, showed significant improvement in glucose and insulin tolerance and reduced body weight, report University of California San Diego School of Medicine researchers.

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.

Chen tested Nobiletin on obese mice with and without a functional clock.

Not exact matches

Human females can live a normal life span with the disease, as can female mice — the latter species also frequently becomes obese.

In the case of the obese mice, Sinclair observes, resveratrol increased insulin levels while decreasing glucose levels, resulting in healthier liver and heart tissue when compared with obese mice that did not receive treatment.

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.

Working together with Cedric Notredame (CRG) and Elena Martín - García (UPF), the scientists found that as well as becoming obese, the mice started very early to show the signs of addiction - like behaviour and binge - eating in response to these enticing foods.

The mice that received the microbiomes of the obese mice gained significantly more weight than did the mice with the lean - mouse microbiomes.

With the risperidone, the mice become obese and exhibit an alternative, less healthy shift in their microbiome,» Kirby says.

«Importantly, we found that blocking the actions of the endocannabinoids with pharmacological inhibitors of cannabinoid receptors in the periphery completely normalized food intake and meal patterns in western diet - induced obese mice to levels found in control lean mice fed standard chow.»

The investigators also discovered that a potent suppressor of autophagy (called mTOR) was hyperactivated in the kidneys of obese mice, and treatment with an mTOR inhibitor ameliorated autophagy insufficiency.

The drug, SRT1720, kept mice with high - calorie diets from becoming obese or diabetic, according to a study published in Cell Metabolism [subscription required].

«Vaccines fail to protect obese mice from severe influenza infections: Fu vaccines with adjuvants don't work as well in obese mice.»

In one recent test, mice implanted with fecal microbes from thin humans stayed thin, while mice given bacteria from obese people gained weight.

Separate groups of germfree mice were colonized with uncultured fecal microbiota from each member of four twin pairs discordant for obesity or with culture collections from an obese (Ob) or lean (Ln) co-twin.

Cohousing mice harboring an obese twin's microbiota (Ob) with mice containing the lean co-twin's microbiota (Ln) prevented the development of increased body mass and obesity - associated metabolic phenotypes in Ob cage mates.

Research conducted at the University of Barcelona showed that obese mice living on a diet enriched with omega - 3s displayed improved sensitivity to insulin.

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).

«The ease with which this weight loss was achieved in mice — even with continued caloric binging — is in stark contrast to the Herculean difficulties morbidly obese patients experience trying to preserve weight loss through dietary restraint,» adds Dr. Gendler.

To identify genes whose expression correlated with adiposity, we profiled gene expression in perigonadal adipose tissue from 24 mice in which adiposity varied due to sex, diet, and the obesity - related mutations agouti (Ay) and obese (Lepob).

Our results indicate that the percentage of macrophages in the adipose tissue that surrounds and infiltrates the extensor digitalis longus muscle is increased in obese mice compared with lean mice.

We examined six experimental groups of 20 - week - old C57BL / 6J mice: (a) lean C57BL / 6J female mice, (b) lean C57BL / 6J male mice, (c) moderately obese C57BL / 6J male mice with diet - induced obesity, (d) moderately obese female B6.Cg Ay / + mice, (e) severely obese female B6.V Lepob / ob mice, and (f) severely obese male B6.V Lepob / ob mice.

Normally, germ - free mice exposed to a mouse with microbial - based obesity would themselves become obese, but we could design a microbial community taken from lean people that protected against this weight gain.

Adipose tissue within muscle contained significant numbers of F4 / 80 + macrophages, and the percentage of F4 / 80 + cells within this adipose tissue was markedly increased in obese mice compared with lean mice (41 % ± 4 % of macrophages vs. 12 % ± 2 % of macrophages, respectively; P < 0.005, mean ± SD)(Figure 4).

Perigonadal adipose tissue was collected from obese B6.V Lepob / ob female mice and digested with a combination of collagenase I and collagenase II.

For example, we showed in collaborative work with Jeffrey I. Gordon's laboratory at Washington University in St. Louis last year that transferring the microbes from an obese person into mice raised in a bubble with no microbes of their own resulted in fatter mice.

To make their discovery, Jin and colleagues used both genetically obese mice and mice with diet - induced obesity as models.

Consistent with their obese phenotype, db / db mice had significantly more visceral white adipose tissue (vWAT), based on comparisons of retroperitoneal fat pad weights relative to body weights at euthanasia [Fig. 2 (a); effect of genotype, F1, 42 = 55.84, P < 0.01].

The percentage of F4 / 80 - positive macrophages within this adipose tissue was markedly increased in obese compared with lean mice (e, P < 0.005).

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.

Surprisingly, the effects of obesity on gut bacteria, inflammation, and osteoarthritis were completely prevented when the high fat diet of obese mice was supplemented with a common prebiotic, called oligofructose.

In 2005, together with Washington University microbiologist Jeffrey Gordon and others, Knight used the tools to catalog the microbes that inhabit the intestines of lean and obese mice, in hopes of uncovering relationships between microbes and metabolic health.

Another important experiment was done later, where they actually bred them across the mice that were knocked out in PTP1B, with mice that were obese, the so - called ob / ob background.

After eight weeks on a high - fat diet, mice that had been engineered with genes to activate the Hedgehog signaling pathway didn't gain weight (left), but control animals whose Hedgehog pathways were not activated became obese (right)(Credit: Long Lab)

Studies in diet - induced obese (DIO) mice with IRAB - A reduced fed blood glucose and insulinemia yet impaired glucose tolerance and led to protracted insulinemia during a meal challenge.

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].

It was shown that the mice with the obese microbiome sample actually extracted MORE calories from the same exact food, gained more weight, and had increased insulin resistance.

Obese mice that ate a high - fat diet along with the green tea compound EGCG (Epigallocatechin -3-gallate) gained weight significantly more slowly compared to a control group of mice which didn't get the green tea supplement.

Also, these mice were in far, far better shape than their obese counterparts with regular myostatin levels.

Researchers inject lab mice, rats, or any kind of animal with MSG, which makes them morbidly obese.

Aids in weight loss Microbe - free mice injected with bacteria from obese people gained weight while mice injected with bacteria from thin people did not.

Green tea -LRB--)- epigallocatechin -3-gallate reduces body weight with regulation of multiple genes expression in adipose tissue of diet - induced obese mice

Their procedure involved infecting mice without microbiota with either microbiota of obese or lean mice.