In her study, «Biological Behavior
of Adipocytes in Adolescents on Depot Medroxyprogesterone Acetate (DMPA): Is It Related to Weight Gain?
Feeding the HF diet markedly induced hypertrophy
of the adipocytes in the epididymal white adipose tissue compared with the control group.
Not exact matches
Differences
in release
of insulin and other pancreatic and gut hormones have also been observed between breastfed and formula - fed infants, with formula feeding leading to higher plasma levels
of insulin which
in turn would stimulate fat deposition and early development
of adipocytes, the cells that store fat (18).
After 2 years as a resident at the University
of Chicago Hospitals, Sargis went to work with Matthew Brady, an endocrinologist
in the University
of Chicago's Pritzker School
of Medicine, studying the development
of adipocytes, the cells that store fat.
Sargis has been working
in Brady's lab for 2 years now, exploring how environmental pollutants influence the molecular programming
of adipocytes.
When macrophages are stimulated with an endotoxin, they produce a factor or factors, termed cachectin, that inhibits the activity
of fat - producing (lipogenic) enzymes
in cultured
adipocytes.
A team led by Antonia Sassmann - Schweda
of the Max - Planck - Institute for Heart and Lung Research and colleagues generated mice lacking TAK1 specifically
in adipocytes.
Adipocytes do indeed secrete more CCL7
in the case
of obesity.
This phenomenon is more frequent
in obese patients,
in whom the size and number
of PPAT
adipocyte cells are higher.
An individual's tendency to be pear or apple - shaped may
in part be set by the ability
of their thigh fat cells to recruit more
adipocytes.
The research team from the Department
of Biochemistry and Molecular Biology headed by Professor Susanne Mandrup are publishing a paper entitled «Browning
of human
adipocytes requires KLF11 and reprogramming
of PPAR super-enhancers»
in the January 1 edition
of the scientific journal Genes & Development that describes their results from working with «brite» fat cells.
UCP - 1 is found
in mitochondria
of adipocytes and plays roles
in converting energy into heat, that is, fat burning.
In humans, most are white adipose tissues, and the
adipocytes contain a large quantity
of neutral fat.
The tissue, called the stroma, includes fat cells, or
adipocytes, that provide padding; fibroblasts, which make the framework for tissue; pericytes
in blood vessels, which are contractile cells that help regulate blood pressure; as well as myoepithelial cells comprising the outer layer
of the ductal system through which milk flows.
«The idea is that when fat cells (
adipocytes) interact with environmental agents —
in this case, bacterial toxins — they then trigger a chronic inflammatory process,» says Patrick Schlievert, Ph.D., UI professor and head
of microbiology and co-senior author
of a new study published
in the journal PLOS ONE.
The accumulation
of adipose tissue macrophages
in direct proportion to
adipocyte size and body mass may explain the coordinated increase
in expression
of genes encoding macrophage markers observed
in our microarray expression data.
Our data
in humans and mice show that
adipocyte size is a strong predictor
of the percentage
of macrophages
in adipose tissue (Figure 3e).
The expression rates
of three macrophage - specific genes (Emr1, Cd68, and Csf1) that correlated with body mass
in our microarray studies, an
adipocyte - specific gene (Acrp30), and proinflammatory genes (Tnfa, Nos2, Il6) were determined by quantitative RT - PCR.
That
adipocytes express receptors for several proinflammatory molecules (e.g., TNF - α, IL - 6) supports models
in which
adipocytes were both the source and target
of proinflammatory signals.
Osteocalcin differentially regulates beta cell and
adipocyte gene expression and affects the development
of metabolic diseases
in wild - type mice
The close relationship between
adipocyte size and the abundance
of macrophages
in adipose tissue suggests that the influence
of adipocyte size on
adipocyte function may be conveyed through a paracrine pathway involving adipose tissue macrophages.
Additionally, I am applying similar strategy to create the
in vitro model
of the inflammation
in adipose tissue using iPS - derived
adipocytes.
Obesity is accompanied by ectopic lipid deposition
in multiple tissues, including the skeleton, where infiltration
of adipocytes into the bone marrow niche may negatively impact bone formation (7, 8).
These data demonstrate that variations
in continuous quantitative traits such as body mass,
adipocyte size, and BMI are correlated with quantitative variations
in the expression
of genes.
Although the slopes corresponding to
adipocyte cross-sectional area for the subcutaneous depot were smaller than (and fell outside the 95 % confidence intervals
of) the slopes for the mesenteric and perigonadal depots, this difference was entirely attributable to the fact that the data from three B6.V Lepob / ob mice fell below the line relating
adipocyte area to macrophage content
in the other animals (Table 1).
In subcutaneous and parametrial adipose tissue, the mean
adipocyte size
of the FVB / NJ Csf1op / op mice (311 ± 71 μm2) was smaller though not significantly different from that
of control FVB / NJ Csf1 + / + mice (476 ± 326 μm2)(P = 0.37).
Average
adipocyte cross-sectional area and the percentage
of F4 / 80 + cells (macrophages)
in adipose tissue depots were determined for each mouse
in this study.
In the extremely obese animals, some
of these macrophage aggregates completely surrounded
adipocytes (Figure 2).
Macrophages
in the adipose tissue
of lean mice were uniformly small, isolated, and widely dispersed among the
adipocytes.
White
adipocytes are mainly located
in the abdominal and subcutaneous areas
of the body and highly adapted to store excess energy.
In mice, both body mass and adipocyte size were strong predictors of the percentage of F4 / 80 + macrophages in the perigonadal, perirenal, mesenteric, and subcutaneous adipose tissue depot
In mice, both body mass and
adipocyte size were strong predictors
of the percentage
of F4 / 80 + macrophages
in the perigonadal, perirenal, mesenteric, and subcutaneous adipose tissue depot
in the perigonadal, perirenal, mesenteric, and subcutaneous adipose tissue depots.
We calculated the average
adipocyte cross-sectional area and the percentage
of F4 / 80 - expressing cells
in the perigonadal, perirenal, mesenteric, and subcutaneous inguinal adipose tissue depots from Ay / + female, Lepob / ob female, lean male, and diet - induced obese (DIO) male mice.
To determine whether adipose tissue macrophages express any molecules implicated
in obesity - associated complications, we isolated three cell populations from the parametrial adipose tissue
of three obese B6.V Lepob / ob mice: (a) an
adipocyte - enriched population, (b) a stromal vascular macrophage F4 / 80 + population, and (c) an F4 / 80 — stromal vascular population.
The researchers selectively ablated Lsd1 and inactivated its catalytic activity
in brown
adipocytes, which triggered a profound whitening
of brown adipose tissue: The colour
of the brown fat cells became paler, their size increased and they started to store energy instead
of expending it.
1,25 - dihydroxyvitamin D3 protects against macrophage - induced activation
of NF?B and MAPK signalling and chemokine release
in human
adipocytes.
PPARγ was initially linked to
adipocyte (fat cell) differentiation, but we now know that it also regulates genes responsible for lipid uptake, accumulation, and storage
of lipids
in those cells.
Isoproterenol Increases Uncoupling, Glycolysis, and Markers
of Beiging
in Mature 3T3 - L1
Adipocytes.
Prolonged decrease
of adipocyte size after rosiglitazone treatment
in high - and low - fat - fed rats.
In his study, Wang found that pups born to mother mice fed a triple dose of Vitamin A were born with more fat - burning brown fat cells, and had more small blood vessels in their adipose tissues, providing precursor cells for energy - burning beige adipocyt
In his study, Wang found that pups born to mother mice fed a triple dose
of Vitamin A were born with more fat - burning brown fat cells, and had more small blood vessels
in their adipose tissues, providing precursor cells for energy - burning beige adipocyt
in their adipose tissues, providing precursor cells for energy - burning beige
adipocytes
N - glycosylation is important for efficient trafficking
of GLUT4 to its proper compartments
in adipocytes (51), suggesting one mechanism by which dysregulation
of these genes could contribute to T2D.
(3,18; cf. 19,20) Even
in visceral fat, it has recently emerged that the obesity - driven rise
in inflammation and insulin resistance is associated with an abnormal accumulation
of senescent cells, albeit senescent endothelial cells rather than
adipocytes.
In individuals with T2D, this function is frequently perturbed by an impaired response of the adipocytes to insulin resulting in elevated lipid levels in circulation and storage in alternative tissues such as liver, muscle, and pancreas (3
In individuals with T2D, this function is frequently perturbed by an impaired response
of the
adipocytes to insulin resulting
in elevated lipid levels in circulation and storage in alternative tissues such as liver, muscle, and pancreas (3
in elevated lipid levels
in circulation and storage in alternative tissues such as liver, muscle, and pancreas (3
in circulation and storage
in alternative tissues such as liver, muscle, and pancreas (3
in alternative tissues such as liver, muscle, and pancreas (3).
The regulation and activatin
of ciliary neurotrophic factor signaling proteins
in adipocytes.
Ferron M, Hinoi E, Karsenty G, Ducy P. Osteocalcin differentially regulates beta cell and
adipocyte gene expression and affects the development
of metabolic diseases
in wild - type mice.
In addition to iPS cells derived from progeria - patients, the researchers successfully applied their method to adult mesenchymal stem cells, which can differentiate into a variety
of cell types, including
adipocytes, osteoblasts, chondrocytes, cardiomyocytes, and, as described lately, beta - pancreatic islets cells.
Complete loss
of mitochondrial CLPP protease protects mice from diet ‐ induced obesity and insulin ‐ resistance but impairs cold ‐ induced thermogenesis due to a decline
in brown
adipocyte function.
Our research focuses on hypothalamic mechanisms necessary for regulating body weight and second the role
of the
adipocyte hormone leptin
in promoting breast cancer.
Joslin scientists are actively involved
in studying the regulation
of the many factors that control the storage, mobilization and utilization
of excess energy
in adipocytes (fat cells).
In 2016 Schulz was appointed head
of the department
of «
Adipocyte Development and Nutrition «at the DIfE, a partner
of the German Center for Diabetes Research (DZD).
After 14 days
of hyperleptinemia,
adipocytes had become shrunken, fatless, and encased
in a thick basement - membrane - like matrix.