The ultrastructural differentiation of brown adipose tissue in the rat

Barnard, Tudor

doi:10.1016/s0022-5320(69)90109-9

Cited by 62 publications

(31 citation statements)

References 15 publications

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“…Cytolysomes (autophagic vacuoles) containing degenerating mitochondria were observed in brown fat cells of rats and newborn rabbits exposed to cold (3-7C) in which fat mobilization was accelerated (NAPOLITANO, 1963;HULL, 1966). BARNARD (1969) observed in brown fat cells of rat fetuses that during birth, especially immediately after birth, a rapid depletion of fat and glycogen took place and autophagic vacuoles became temporarily numerous. This evidence suggests the role of autophagic vacuoles during periods of enhanced fat consumption for local heat production.…”

Section: Electron Microscopic Observationsmentioning

confidence: 93%

“…BARNARD (1969) and SUTER (1969a) demonstrated that, in immature brown fat cells of rat fetuses, glycogen particles accumulated prenatally, but were depleted within several hours after birth. This glycogen depletion and repletion in brown fat cells have been examined in cold-exposed and coldacclimated rats (SUTER, 1969b;THOMSON et al, 1969).…”

Section: Electron Microscopic Observationsmentioning

confidence: 99%

“…FAWCETT (1952) and NAPOLITANO (1965) proved that in adult rats the glycogen content in adipose tissue depended on the nutritional and endocrine (insulin) state of the animal. In fat synthesizing adipose cells, it has been proved that glycogen particles and fat droplets simultaneously appear and increase (BARNARD, 1969;SUTER, 1969b). GIESEKING (1961) has claimed that glycogen particles can be transformed into lipid in brown fat cells of the mouse.…”

Section: Electron Microscopic Observationsmentioning

confidence: 99%

“…The question of whether lipid droplets in fat cells have a limiting membrane or not has remained a matter of controversy. Some authors have denied the existence of the membrane (NAPOLITANO, 1965;LINDBERG et al, 1967;SUTER, 1969b;THOMSON et al, 1969), while others, such as PICARD et al (1966), UMAHARA (1968) and BARNARD (1969) have demonstrated its existence. Especially LICKENBILL and COHEN (1966), IMAIZUMI (1967) and WOOD (1967) recognized, at the fat droplet-cytoplasmic interface, a meshwork composed of about 70 (80)-100 A thick filaments.…”

Section: Electron Microscopic Observationsmentioning

confidence: 99%

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Morphological studies on brown adipose tissue in the bat and in humans of various ages.

Ito

Tanuma²,

Yamada³

et al. 1991

Arch. Histol. Cytol.

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Section: Electron Microscopic Observationsmentioning

confidence: 93%

Section: Electron Microscopic Observationsmentioning

confidence: 99%

Section: Electron Microscopic Observationsmentioning

confidence: 99%

Section: Electron Microscopic Observationsmentioning

confidence: 99%

See 2 more Smart Citations

Morphological studies on brown adipose tissue in the bat and in humans of various ages.

Ito

Tanuma²,

Yamada³

et al. 1991

Arch. Histol. Cytol.

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“…Wild-type EWAT consisted of well-developed adipocytes with a single lipid droplet in the cytoplasm. In contrast, EWAT derived from ∆80 and ∆98 mice had a fetal/perinatal appearance, with abundant WAT precursors, without evidence of de-lipidated mature adipocytes (22). A peculiar EM finding was the presence of enlarged mitochondria with large electron-dense inclusions (Figure 4, b-d).…”

Section: Generation Of Insr Mosaicsmentioning

confidence: 95%

Mosaic analysis of insulin receptor function

Kitamura

Kitamura²,

Nakae³

et al. 2004

J. Clin. Invest.

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Insulin promotes both metabolism and growth. However, it is unclear whether insulin-dependent growth is merely a result of its metabolic actions. Targeted ablation of insulin receptor (Insr) has not clarified this issue, because of early postnatal lethality. To examine this question, we generated mice with variable cellular mosaicism for null Insr alleles. Insr ablation in approximately 80% of cells caused extreme growth retardation, lipoatrophy, and hypoglycemia, a clinical constellation that resembles the human syndrome of leprechaunism. Insr ablation in 98% of cells, while resulting in similar growth retardation and lipoatrophy, caused diabetes without β-cell hyperplasia. The growth retardation was associated with a greater than 60-fold increase in the expression of hepatic insulin-like growth factor binding protein-1. These findings indicate that insulin regulates growth independently of metabolism and that the number of insulin receptors is an important determinant of the specificity of insulin action. Conflict of interest:The authors have declared that no conflict of interest exists. Nonstandard abbreviations used: insulin receptor (Insr); forkhead transcription factor o1 (Foxo1); insulin-like growth factor binding protein-1 (Igfbp1); phosphatidylinositol-tris-phosphate (PIP3); pancreatic and duodenal homeobox protein-1 (Pdx1); peroxisome proliferative activated receptor, γ, coactivator 1α (Pgc1α); heat shock promoter (HSP); HSP 70-1 Cre transgenic (Hs-Cre6); growth hormone (GH); triglyceride (TG); 125 I-labeled insulin ( 125 I-insulin); 125 I-labeled IGF2 ( 125 I-IGF2); brown adipose tissue (BAT); phosphoenol-pyruvate carboxykinase (Pck1); glucose-6-phosphatase (G6pc); hepatic glucose transporter Glut2 (Slc2a2); glucokinase (Gck); sterol regulatory element binding transcription factor-1 (Srebf1); glycogen synthase (Gys1); glycogen phosphorylase (Pygl); phosphofructokinase, liver (Pfkl); forkhead transcription factor a2 (Foxa2); uncoupling protein-1 (Ucp1); peroxisome proliferator activator receptor γ (Pparγ); adrenergic β3 receptor (Adrb3).

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The development of the elastic cartilage of the mouse pinna

Sanzone

Reith

1976

Am. J. Anat.

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The development of the elastic cartilage in the mouse pinna was studied with the electron microscope. For descriptive purposes, the developmental process was divided into five stages. These begin with the onset of cartilage matrix production by chondroblasts. The second stage is the major mitotic stage although the cells now resemble chondrocytes and cartilage matrix production evidently continues. This is followed by a period during which cartilage matrix production appears to be the major activity of the chondrocytes. In Stage IV, the cells continue to produce cartilage matrix but at the same time they also produce lipid which comes to occupy most of the cell as a large lipid droplet. In the adult, Stage V, matrix production appears to be at an end and each cell contains a lipid droplet which is so large that the cells bear some resemblance to white fat cells and might be designated as lipochondrocytes. The adult cartilage matrix contains elastic plates in a three-dimensional honeycomb pattern. Between the elastic plates and the cells, the matrix contains elements similar to those seen in hyaline cartilage but it does not contain matrix vesicles such as those which have been associated with the calcification of cartilage. Two types of filaments differing in appearance, size, and location are seen within the chondrocytes. They have been designated cytofilaments and cortical filaments. Cytofilaments are dispersed throughout the cell and also contact the substance of the lipid droplet; cortical filaments (sub-plasmalemmal microfilaments) are located directly under the plasma membrane. They are thought to be involved in movement of the plasma membrane as a concomitant to extracellular fibrogenesis.

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The ultrastructural differentiation of brown adipose tissue in the rat

Cited by 62 publications

References 15 publications

Morphological studies on brown adipose tissue in the bat and in humans of various ages.

Morphological studies on brown adipose tissue in the bat and in humans of various ages.

Mosaic analysis of insulin receptor function

The development of the elastic cartilage of the mouse pinna

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