Key result
Denervation of brown fat lobes in mice led to cell hypertrophy due to lipid accumulation, transient glycogen increase, and a decreased capillary bed indicative of reduced blood flow.
Denervation of brown adipose tissue in mice leads to cellular hypertrophy from lipid accumulation and reduced capillary blood flow.
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Should not alter clinical adipose management; leaves open sympathetic control of human brown fat vascularity.
Intact and denervated brown fat lobes of normal and cold‐exposed mice were studied by light and electron microscopy. Following two weeks of denervation in normal and cold‐exposed mice, denervated brown fat cells were hypertrophied because of lipid accumulation. In normal mice there was a transient increase in glycogen. In cold‐exposed mice, the quantity of glycogen in intact and denervated brown fat was greater than in normal mice. Mitochondria increased in size, and the number of cristae was greater in intact fat of cold‐exposed mice than in denervated brown fat. Carbon perfusion of blood vessels demonstrated a decreased capillary bed in denervated fat. Capillary constriction noted only in denervated brown fat is indicative of reduced blood flow.
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Slavin et al. (1974) studied Normal and cold-exposed mice. Denervation of brown fat lobes vs. Intact brown fat lobes was evaluated on Morphological changes (hypertrophy, lipid accumulation, glycogen, mitochondria size, capillary bed). Denervation of brown fat lobes in mice led to cell hypertrophy due to lipid accumulation, transient glycogen increase, and a decreased capillary bed indicative of reduced blood flow.
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