White Fat Cells Research Articles

Morphological features of brown adipose cell maturation in vivo and in vitro.

AbstractThe maturation of brown adipose cells, derived at various time intervals from interscapular brown fat pads of neonatal rats, has been investigated electron microscopically. The major changes in in vivo brown adipose cells are related to lipid accumulation. In older animals, fat droplets are separated by a membrane complex, and membranous fragments are seen within large lipid inclusions. The ultrastructural characteristics of monolayer cultures of brown fat cells, isolated from neonatal brown fat pads by tryptic dissociation, and maintained for one to six days on a reconstituted collagen matrix, have also been investigated. Adipose cells in vitro are morphologically similar to control brown fat cells, and lipid accumulation closely parallels that seen in vivo. In vitro lipid droplet coalescence, impossible to visualize in vivo, has been documented by time‐lapse cinematography, and membrane complexes similar to those observed in vivo are seen. Major changes in cultivated fat cells, compared to in vivo cells, involve extensive glycogen deposition and breakdown of cytoplasmic ribosomal rosettes. Older cultures contain adipose cells exhibiting characteristics of white fat cells. Effects of tissue culture environment upon the brown fat cells, and the possible conversion of the brown fat cell into a white fat cell are discussed.

Effect of dibutyryl-3',5'-AMP, theophylline and norepinephrine on lipolytic action of growth hormone and glucocorticoid in white fat cells.

The lipolytic action of growth hormone and glucocorticoid on white fat cells was affected by catecholamines and theophylline. Growth hormone and glucocorticoid produced a 5- to 10-fold increase in the sensitivity of fat cells to norepinephrine or theophylline without affecting the maximal response. Dibutyryl-3′,5′-AMP also stimulated fat cell lipolysis but growth hormone and glucocorticoid actually inhibited its lipolytic action. The ability of growth hormone and glucocorticoid to increase the sensitivity of fat cells to theophylline was abolished by cycloheximide, an inhibitor of protein synthesis. These results suggest that growth hormone stimulated the synthesis of a protein involved in the formation but not in the action of 3′,5′-AMP. (Endocrinology 82: 825, 1968)

Light and electron microscopic studies on the brown adipose tissue in the bat.

In the bat, Rhinolophus ferrum-equinum nippon, captured monthly throughout the year, the interscapular brown fat was observed by light and electron microscopy to elucidate ultrastructural characteristics and the seasonal changes of this tissue.1. The brown fat cells are smaller than the monolocular cells of the common white fat. They are characterized by the multilocularity of the cytoplasm caused by the occurrence of many lipid droplets and by abundant, closely packed mitochondria of large size with compact and parallel cristae. Monolocular fat cells resembling those of the white fat tissue and transitional forms between the former and the typical multilocular brown fat cells were not infrequently observed. This finding was not interpreted to support the view that the brown fat cells might be converted into the white fat cells, since it was revealed that the monolocular and transitional cells found in the brown fat retained certain morphological characteristics of brown fat cells.2. Conspicuous seasonal changes were revealed in the brown adipose tissue of the bat: Extensive repletion of brown fat cells with lipid droplets during autumn months (September, October and November) and an unexpectedly inconspicuous fat depletion during hibernation (December, January, February and March) were proved. A strong depletion of fat droplets from brown fat was found in April suggesting that this month might correspond to the arousal period of the bat. The strongest diminution of fat droplets accompanied by conspicuous atrophy of brown fat cells was confirmed in August bats. This change was correlated to a possible resting stage of the brown fat tissue as a heat producing organ in this season of constant and high ambient temperature.3. In the cytoplasm of brown adipose cells of the bat there occured besides closely packed mitochondria and multiple lipid droplets bounded by a smooth limiting membrane, occasional centriole, a number of small Golgi complexes scattered randomly, numerous clusters of free ribosomes, pinocytotic invaginations and vesicles, and elements of agranular endoplasmic riticulum; elements of granular endoplasmic reticulum and glycogen particles were missed. Cytolysomes of different contents and structures and certain types of dense bodies including probably lysosomes were distinguished and described in detail.4. The fat synthesis in brown adipose cells is suggested to take place within the tubules and vesicles of the agranular endoplasmic reticulum distributed extensively in the cytoplasm. This view is supported by the finding that these structures often contain osmiophilic homogeneous material which is believed to be lipid substance.5. Occasional small cells of an unknown nature were found in the concavities on the surface of the brown fat cells. These cells contained a small nucleus, sparse small mitochondria and irregularly shaped dense bodies of variable sizes.6. Capillaries distributed richly between fat cells were, in their cross section, lined by one, two, three or several endothelial cells. The perikaryon of the capillary endothelium possessed a diplosome within the paranuclear Golgi area. Cross striated rootlets protruded from the paired centrioles of the diplosome were demonstrated and shown to be composed of closely packed, parallel filaments.7. Small unmyelinated nerve bundles were identified between brown fat cells and near the capillaries and varicose thicknings of unmyelinated nerve fibers forming synaptic contacts with brown fat cells and capillaries contained, besides occasional large granular vesicles measuring about 700-890A in diameter, numerous small granular or cored (420-540A in diameter) and agranular or empty (210-260A) vesicles (and tubules). The former type of the small vesicles seems to correspond to the so-called granular synaptic vesicles characteristic of adrenergic nerve endings.

Inhibition of lipolytic action of growth hormone and glucocorticoid by ultraviolet and x-radiation.

Addition of catecholamines or growth hormone plus glucocorticoid activates lipolysis in isolated white-fat cells of the rat. If the fat cells were irradiated just before the addition of growth hormone and glucocorticoid, their lipolytic action was abolished. However, irradiation did not affect the activation of lipolysis by catecholamines.

The Isolation and Metabolism of Brown Fat Cells

Abstract A procedure is described by which free brown fat cells can be obtained from the dorsal interscapular brown fat of rats. The brown fat cells accounted for less than 25% of the cells present in the intact tissue. The ratio of triglyceride to nitrogen in brown fat cells was about 10% of that in white fat cells. Growth hormone and 9α-fluoro-11β, 17α,21-trihydroxy-16α-methyl-1,4-pregnadien-3,20-dione (dexamethasone) did not accelerate brown fat cell lipolysis. The response of brown fat cells to adrenocorticotrophic hormone was less marked than that of white fat cells. However, the dose-response curve for stimulation by epinephrine of glycerol or fatty acid release in brown fat cells was similar to that observed in white fat cells. Epinephrine markedly stimulated oxygen consumption by brown fat cells. The Qoo2 for brown fat cells (based on lipid-free dry weight) was greater than 100 in the presence of epinephrine. Brown fat cells utilized considerably more free glycerol for re-esterification of fatty acids than did white fat cells. The conversion of labeled glycerol to carbon dioxide and fatty acid by brown fat cells was much greater than that by white fat cells and was unaffected by insulin. The metabolism of glucose by brown fat cells increased progressively over an 8-hour incubation period and was not inhibited by dexamethasone. Insulin accelerated the metabolism of glucose by brown fat cells and also decreased the stimulation of both fatty acid and glycerol release by epinephrine in either the presence or absence of glucose. Epinephrine increased glucose conversion to glyceride glycerol only in the presence of insulin.

Aspect ultrastructural de la lipog�n�se dans le tissu adipeux brun

In interscapular brown fat of the rat, appropriately processed so as to maintain membrane structures intact, lipid droplets are in fact liposomes, i.e., lipid filled vacuoles surrounded by a membrane that is related to the smooth endoplasmic reticulum. Thus the endoplasmic reticulum appears as an important component of brown fat cells. — After complete lipid depletion has been achieved by 7 days of fasting, feeding with glucose results in sudden and very conspicuous increase of smooth endoplasmic reticulum; dilatations of the perinuclear cistern and pinocytotic activity at the periphery of the cell contribute to this increase. Simultaneously the cytoplasmic matrix is heavily loaded with glycogen in particulate form. Lipogenesis, as far as can be appreciated by different degrees in electron density, takes place inside the vesicles of the endoplasmic reticulum; increase of such small lipid vacuoles then leads to reconstitution of liposomes; return to the normal aspect is completed 12 hours after the beginning of feeding. — During the phase of glycogen overloading and resulting lipogenesis, glycogen particles may be found in intercellular and pericapillary spaces; the significance of this finding is discussed. — The fundamental difference between both types of fat cells seems to be concerned with the site of lipogenesis: this takes place in the cytoplasmic matrix of white fat cells, so that lipid droplets aggregate without any limiting membrane, whereas in brown fat cells lipogenesis occurs inside cavities of the endoplasmic reticulum and lipids remain permanently enclosed in membranes. This process appears similar to what may be observed occasionally in liver and normally in adrenal cortex, and this might presumably lead to a physico-chemical understanding of the particular aspect of lipogenesis in brown fat, as compared to that in common white fat.

Influence of cortisone upon brown fat of hamsters and mice.

Summary1. Beyond an early age (about 3 weeks), the proportion of brown fat within the hamster maintains a relative constancy. In contrast, the ratio of white fat to body weight increases precipitously with age until full maturity of the hamster. 2. Cortisone treatment results in a prompt hypertrophy of brown fat in hamsters and mice, reflected microscopically by measurable expansion of cell diameter. White fat is possibly somewhat reduced in weight. 3. The reactive hypertrophy of brown fat in cortisone-treated hamsters diminishes with increasing age, apparently caused in part by the increasing numbers of unresponsive white fat cells within the borders of brown fat masses.