White adipose tissue was obtained from the mesentery, epididymis, omentum and subcutis of rats which were fed, fasted or fasted and then refed. Tissue samples were prepared using the glyoxylic acid method to detect adrenergic nerves by fluorescence histochemistry. Other tissue samples were fixed with an aldehyde solution containing sodium molybdate which is specific for catecholamine granules in nerve terminals. Thin and serial thick sections (0.25-0.5 micron) were viewed with a conventional electron microscope and with the high voltage electron microscope. With fluorescence microscopy it was found that most of the blood vessels except veins and venules were richly innervated. The most extensive branching of nerves down to the capillary level was found in the mesentery and epididymal fat of fasted-refed rats. Relatively few adipocytes appeared to be innervated. With electron microscopy, nerve terminals were found distributed with most blood vessels including capillaries, and with some adipocytes. Only 2-3% of all dipocytes were innervated by adrenergic nerves. It is suggested that in the adipose tissue sites studied the major adrenergic innervation is mainly for the supply of blood vessels.

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The differentiation of mammalian white adipocytes from prenatal through early postnatal periods was studied by light and electron microscopy in C57BL mice. Anatomical regions chosen for this study were the epididymal, mesometrial, mesenteric and inguinal fat pads. In each of these regions, adipocytes differentiated from fibroblast-like cells (preadipocytes) characterized by a n ovoid nucleus, profiles of rough endoplasmic reticulum, microtubules, microfilaments, spherical mitochondria, and small multiple lipid inclusions. Preadipocytes of the inguinal fat pad were first observed prior to birth (17-19 days), whereas, in the other anatomical sites, these cells were not observed until one to three days postnatally. As differentiation proceeded, and as the adipocytes assumed a spherical shape, there was a progressive decrease in the amount of rough endoplasmic reticulum and microfilaments concomitant with transient glycogen storage and a n increase in the size of lipid droplets. Mature unilocular adipocytes were observed in the inguinal fat pads a t three days of age. On the other hand, these cells did not appear until seven days after birth in the epididymal fat pad, mesometrium and mesentery. Regardless of the anatomical region studied, the differentiation of preadipocytes to adipocytes proceeded similarly. Preadipocytes could not be distinguished from fibroblasts morphologically within the fat depots studied. Adipocytes a t the mid-stages of differentiation and in all regions studied occasionally exhibited close intercellular contacts of varying morphology.The differentiation of mammalian white adipocytes has been extensively studied by light microscopy with considerable debate concerning the nature of the adipocyte precursor (Clark and Clark, '40; McCullough, '44; Tedeschi, '60; Barrnett, '62; Wasserman, '64; Simon, '65; Tavassoli, '76). Napolitano ('63) was the first investigator to demonstrate by electron microscopy t h e development of adipocytes in the rat. Recently, Desnoyers and Vodovar ('77) compared the fine structural development of adipocytes in pigs and rats. In these studies, the adipose depots were fixed solely in osmium tetroxide. The present paper reevaluates the specific morphologic and cytologic changes occurring during adipocyte development by the use of primary aldehyde fixation which allows for the demonstration of several cytologic features previously undescribed. MATERIALS AND METHODSAdipocytes from the epididymal, mesometrial, mesenteric and inguinal fat pads were studied following routine immersion fixation in 3% glutaraldehyde and 1% formaldehyde buffered with sodium cacodylate (0.1 M), pH 7.2. The tissues were obtained from eight male and eight female C57BL mice varying in age from 17 days prenatal to 7 days postnatal. Blocks of tissue were postfixed in 1% osmium tetroxide, dehydrated in ethanol and embedded in Spurr's low-viscosity epoxy resin or in an Epon-Araldite mixture. Routine thick sections (1 pm) were cut and stained with silver according to the procedure of Rosenquist et al.(...

The fatty liver dystrophy ( fld ) mutant mouse is characterized by neonatal fatty liver and hypertriglyceridemia that resolve at weaning, and neuropathy affecting peripheral nerve in adulthood. We now report additional significant manifestations of this single gene mutation, which include adipose tissue deficiency, glucose intolerance, and increased susceptibility to atherosclerosis. In adult fld/fld mice, both white and brown fat pads exhibit an 80% reduction in mass compared with wild-type controls, and consist of immature adipocytes as assessed by morphological and molecular criteria. The lack of lipid accumulation in fld/fld adipose tissue could be attributed, in part, to a failure to induce expression of lipoprotein lipase and enzymes involved in fatty acid synthesis, such as fatty acid synthase and acetyl-CoA carboxylase. Related to the deficiency of adipose tissue, fld/fld mice were also found to exhibit profound glucose intolerance, modest hyperinsulinemia, and reduced tissue response to insulin. As insulin resistance is a important risk factor in vascular disease, we examined susceptibility of fld/fld mice to diet-induced atherosclerosis. Mutant mice fed an atherogenic diet developed 2-fold greater aortic lesions than their wild-type counterparts, despite having a less atherogenic lipoprotein cholesterol profile. The fld adipose-deficient phenotype has both similarities to and distinctions from the group of rare human diseases known as lipodystrophies. -Reue, K., P. Xu, X-P. Wang, and B. G. Slavin. Adipose tissue deficiency, glucose intolerance, and increased atherosclerosis result from mutation in the mouse fatty liver dystrophy ( fld ) gene.