Biomedical subjects
Publications and source records attributed to B Cannon.
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1. Brown adipose tissue of the hamster possesses high specific activities of soluble, cytoplasmic NAD-linked, as well as mitochondrial flavin-coupled, glycerol-3-phosphate dehydrogenases. The ratio of the two enzyme activities is high (close to 1), when compared with other tissues of the hamster. 2. In the presence of rotenone, NADH is oxidised very poorly by homogenates of brown adipose tissue. A high rate of oxidation is obtained upon further addition of dihydroxyacetone phosphate, which itself is negligible oxidised. When followed fluorimetrically glycerol 3-phosphate can also be observed to induce NADH oxidation, but only after a significant lag time. Similar results are obtained with isolated mitochondria plus high-speed supernatant. With high-speed supernatant alone, only dihydroxyacetone phosphate has any effect, whereas with isolated mitochondria neither dihydroxyacetone phosphate nor glycerol 3-phosphate induce any NADH disappearance. 3. Respiration induced by NADH plus dihydroxyacetone phosphate in homogenates equals 56% of the respiration induced by glycerol 3-phosphate alone. 4. Respiration induced by NADH plus dihydroxyacetone phosphate, as well as that induced by glycerol 3-phosphate, is inhibited by the same concentrations of inhibitors as are required for inhibition of the mitochondrial dehydrogenase i.e. EDTA, long-chain unsaturated fatty acids, long-chain fatty acyl CoA esters. 5. In isolated brown adipocytes in the presence of rotenone, norepinephrine significantly inhibits respiration induced by glycerol 3-phosphate. 6. The results obtained are discussed with respect to the role of glycerol 3-phosphate as an electron sink for cytosolic reducing equivalents to maintain a low level of extramitochondrial NADH. A means of maintaining a level of glycerol 3-phosphate adequate for triglyceride synthesis is also considered.
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A technique was developed to produce small intestinal mucosal injury in vivo by perfusing the mid-small intestine of rats with HCl, NaOH, FeSO4, and AgNO3. Three hours following injury, gastric emptying and small intestinal transit were measured by examining the gastrointestinal distribution of a non-absorbable radioisotope which had been placed in the stomach for 1 hour. There was a strong association between the villus injury produced by various concentrations of the injurious agents and the degree of gastric retention. Necrosis of villus tips, as produced by AgNO3, was sufficient to cause marked gastric retention. Injury to the small intestinal mucosa of one parabiotic rat did not produce gastric retention in the partner. It is concluded that injury to small intestinal villi is sufficient to induce gastric retention and that the effect is most likely nerve-mediated.
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Epididymal adipose tissue in the rat is generally considered to be "pure" white adipose tissue (WAT) with a characteristic structure and function. Previous studies in cats have, however, indicated that adipose tissue with the morphological appearance of WAT could be converted into a tissue with the morphological appearance of brown adipose tissue (BAT) by intermittent cold stress. The present electron microscopic and morphometric study describes the effect of intermittent cold stress on the epididymal WAT of young rats. The tissue volume decreased markedly as did the lipid content. The mitochondrial volume increased dramatically. The extracellular matrix was vastly reduced as was the thickness of the plasma membrane, and the number of gap junctions between adipocytes increased markedly. Indications of neoinnervation and neovascularization were observed. A great abundance of preadipocytes indicated proliferative activity of the endothelium. The low amount of lipid droplets and a relative abundance of smooth and rough endoplasmic reticulum. Golgi apparatus, and lysosomes in the epididymal WAT of cold-stressed rats gave the cells the morphological appearance of young adipocytes or preadipocytes whereas the hypertrophic and hyperplastic mitochondria, the relative paucity of ribosomes on lipid droplet membranes, and the increased innervation and vascularization gave the cells the morphological characteristics of brown adipose tissue.
We have previously shown that after severe cold stress of rats the epididymal white adipose tissue (WAT) acquires many of the morphological characteristics (innervation, vascularization, appearance of adipocytes) of brown adipose tissue (BAT). In the present study, the mitochondrial characteristics have been analyzed. Mitochondria from the epididymal fat pad of cold-stressed rats became enlarged and had a volume 1.7 times greater than that in the control group (0.5 microns 3 in the experimental versus 0.3 microns 3 in the control group). The mitochondria occupied about 60% of the cytoplasm (14% in the control group), thus approaching the highest value reported for any cell. The straight or slightly wavy cristae completely traversed the width of the mitochondria and occupied an area of 26 microns 2/1 microns 3 of mitochondrion in the experimental adipose tissue (7 microns 2 in the control group) and 15 microns 2/1 microns 3 of cytoplasm (1.4 microns 2 in the control). The mitochondrial matrix became electron lucid and could contain lamellar whorls, as could the surface of the mitochondria. These mitochondria of epididymal WAT resembled, both morphologically and morphometrically, mitochondria in the BAT of cold-exposed rodents. In the epididymal mitochondria, immunoelectron microscopy did not reveal the presence of the BAT-specific uncoupling protein thermogenin, nor could the slot-blot technique detect thermogenin mRNA. We conclude that even under these extreme conditions of cold stress, WAT cannot adopt the thermogenin-dependent thermogenesis of BAT. The dramatic mitochondriogenesis can be interpreted only as being indicative of an extremely high metabolism in the tissue, thus placing unprecedented pressure on the energy turnover capacity of the cell.
Young cats (Felis domestica), aged 10-13 weeks, were intermittently exposed to a temperature of -30 degrees C for two periods of 1 hr per day. Animals were sacrificed on the 7th day and adipose tissue from the perirenal, pericardial, axillary, interscapular, and subcutaneous-inguinal depots was examined by electron microscopy and analysed stereologically. All examined depots were morphologically changed after cold treatment. Adipose tissue of perirenal, pericardial, and axillary depots showed a greater decrease in lipid content than the interscapular and subcutaneous-inguinal depots, but other changes were similar. Compared to the control group, which consisted of typical white adipose tissue, the diameter of adipose cells examined after cold treatment was diminished, in extreme cases to 18 micron (from 75 micron in the control group). The number of capillaries per cell was doubled (as evaluated on semithin sections). The most dramatic changes were observed in the mitochondria. Their volume increased to 0.48 micron 3 (from 0.13 micron 3 in the control), and the surface density of mitochondrial cristae per mitochondrial volume increased to 50 micron 2/micron 3 (from 32 in the control). Pleomorphism in mitochondrial size and inner structure and the presence of intramitochondrial electron-dense bodies and crystalline structures led us to conclude that the cold stress induced an increase in the absolute number of mitochondria in the adipose cells. The adipose tissue after cold treatment thus morphologically resembled the brown adipose tissue of cold-acclimated rodents. This implies that the adipose tissue of young cats can change its morphology and function, depending on the requirements of the organism.