Lori Shemek, Ph.D. is a leading
fat cell researcher and recognized authority on inflammation and its role in weight loss, preventing disease and optimizing health.
Not exact matches
One preliminary
cell study by
researchers at Sejong University in South Korea found that piperine may impact
fat cells.
«
Researchers watch in real time as
fat - encased drug nanoparticles invade skin
cells.»
The
researchers collected samples of indoor dust from 11 homes in North Carolina and tested extracts from the samples in a mouse pre-adipocyte
cell model, 3T3 - L1
cells, often used to test compounds for potential effects on the accumulation of triglycerides, a type of
fat.
This suggests that the mixture of these chemicals in house dust is promoting the accumulation of triglycerides and
fat cells, the
researchers say.
The
researchers explain that a high
fat diet boosts
cell metabolism, including the release of inflammatory chemicals, as well as influencing the gut microbiome and associated immunity.
«
Fat cells can adopt a range of metabolic phenotypes, depending on physiological conditions and location in the body,» said James G. Granneman, Ph.D., a
researcher involved in the work from the Center for Integrative Metabolic and Endocrine Research at the Wayne State University School of Medicine in Detroit, MI.
The
researchers found that they could trigger the same effects in healthy muscle
cells by exposing them to the
fat palmitate.
Researchers at the University of Memphis and University of Pennsylvania report the development of robust new liver and
fat cell models that report circadian clock function.
It appears to work by adjusting the body's metabolism, allowing muscles to favor burning
fat over sugar,
researchers report in the May 2
Cell Metabolism.
Using human - derived glioblastoma
cells in a mouse models,
researchers found that the modified high -
fat, low - carbohydrate diet increased life expectancy by 50 percent while also reducing tumor progression by a similar amount.
After reading Morrison's work, Siddaraju Boregowda, a stem
cell researcher at the Scripps Research Institute in Jupiter, Florida, was reminded of genetically altered mice that don't gain body
fat or develop diabetes, even when fed high -
fat diets.
He and his boss, stem
cell researcher Donald Phinney, wondered whether those mice were also protected from the fattening of the bone marrow that accompanies a high -
fat diet.
The plant compounds used by the UGA
researchers — resveratrol, found in grapes; genistein, found in soybeans; and quercetin, found in apple peels and onions — have all been shown in previous studies to be
fat - busters, causing
fat cells to burst and release their contents.
Components of indoor dust may signal human
fat cells to grow and may alter metabolism, potentially contributing to weight problems,
researchers report July 14 in Environmental Science & Technology.
The
researchers obtained stem
cells from the discarded
fat of liposuction patients who underwent elective surgery.
As a patient's BMI increases,
fat cells communicate with multiple myeloma
cells,
researchers found.
Now, Salk
researchers have discovered how the molecule ERRγ gives this «healthier» brown
fat its energy - expending identity, making those
cells ready to warm you up when you step into the cold, and potentially offering a new therapeutic target for diseases related to obesity.
Harvard Medical School
researcher Melina Claussnitzer and her team found that a single variation in the FTO gene caused
fat cells that would normally become healthier beige to turn into white
fat cells instead.
Researchers previously thought that
fat cells were mostly responsible for making lipocalin 2, or LCN2.
Now
researchers from the University of Southern Denmark have uncovered the mechanism by which white
fat cells from humans get reprogrammed to become browner.
The UI
researchers used immortalized
fat cells to show that bacterial toxins stimulate
fat cells to release molecules called cytokines, which promote inflammation.
To determine how
fat might alter glucose uptake, the
researchers measured the production of blood - borne molecules that
fat cells secrete.
By 1999
researchers from Japan's National Cardiovascular Center Research Institute in Osaka had announced the discovery of ghrelin, a kind of antileptin that is released primarily by the gut rather than by
fat cells.
Researchers have turned their attention to these
cells because some of the sugar and
fat they burn is stored in the body and might otherwise lead to increases in white
fat, the form that increases in obesity.
The
researchers used the new lab - on - a-chip to study how adult stem
cells in adipose tissue develop into mature
fat cells, conducting their investigations outside the body.
Harvard School of Public Health (HSPH)
researchers have discovered that a particular type of protein (hormone) found in
fat cells helps regulate how glucose (blood sugar) is controlled and metabolized (used for energy) in the liver.
The
researchers were surprised to find that knockdown of one specific mitochondrial chaperone, mtHSP70, elicited a unique stress response mediated by
fat accumulation, resulting in improved protein folding in the interior or cytosol of the
cell.
The
researchers tested two anti-CK2 drugs for their ability to stimulate the production of new brown
fat in mice: a new small - molecule CK2 - blocker called silmitasertib (CX - 4945), which is already in clinical trials as a cancer therapeutic; and a more precise next - generation antisense oligonucleotide (ASO) drug developed in collaboration with Isis Pharmaceuticals, which eliminates CK2 by blocking the RNA instructions
cells use to produce it.
This is more than a mere change of color, as the
researchers also found that these bile acids increase the number of mitochondria in the new
fat cells.
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 day.
The
researchers now want to find out exactly how Tregs interact with
fat tissue and whether the immune
cells accumulate in other organs during normal aging.
Researchers at the University of Michigan have identified how a promising drug in clinical trials for the treatment of obesity and related metabolic disorders improves the metabolism of sugar by generating a new signal between
fat cells and the liver.
Given the similar results, the
researchers believe that
fat cells plus SVF are preferable to stem
cell injection.
By collecting samples from three different groups of patients, the
researchers were able to compare the health of the precursor
fat cells of the three groups.
The defect in the creation of the
fat cells means that the women's bodies are more likely to have problems using blood sugar, the
researchers found.
RIPK1, the
researchers found, inflicts damage by directly attacking the body's myelin production plants — nerve
cells known as oligodendrocytes, which secrete the soft substance, rich in
fat and protein that wraps around axons to support their function and shield them from damage.
The
researchers discovered that one strain had a genetic defect in
fat cells that secrete a hormone called leptin.
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.
While doctors, nutritionists and
researchers have known for a long time that saturated
fats contribute to some of the leading causes of death in the United States, they haven't been able to determine how or why excess saturated
fats, such as those released from lard, are toxic to
cells and cause a wide variety of lipid - related diseases, while unsaturated
fats, such as those from fish and olive oil, can be protective.
Researchers scanned the brains of two voracious teenagers whose
fat cells were unable to secrete leptin normally, but after being given the hormone for a week became pickier eaters.
In others, the
researchers altered a gene that regulates phospholipids, the primary type of
fat in
cell membranes, which spurred the
cells into producing more cholesterol on their own.
In the current study, published in
Cell Reports, the
researchers investigated the relationship between p75 NTR and a diet high in
fat — often the cause of these problems.
As the
researchers have shown in various studies on mice, the widespread active ingredient sildenafil or a medication against pulmonary hypertension, for instance, can be used to reduce the number of white
fat cells to the benefit of the brown
fat cells and thus accelerate
fat burning like a turbocharger.
In the 1990s,
researchers tried using a virus or
fat particles to insert the correct CFTR gene into patients» lung
cells.
The
researchers posit the explanation that kynurenic acid activated the
cell receptor GPR35, which is found in both
fat cells and immune
cells.
If the
researchers» dream comes true, brown
fat cells could be boosted with yet - to - be-developed active substances such that rolls of
fat could simply be melted off.
The
researchers observed that there is a particularly high number of receptors in brown
fat cells which bind to the Gq protein.
In a recent study, the university
researchers show why the inflammatory responses that often occur in overweight people block this kind of
fat cell conversion.
Their ability to remain diabetes - free,
researchers have now discovered, can be chalked up to the shutting down of a protein found in
fat cells.