Lipid metabolism: Effects of immunosympathectomy and acclimation to cold

1968 ◽  
Vol 46 (3) ◽  
pp. 453-461 ◽  
Author(s):  
G. Steiner ◽  
E. Schönbaum ◽  
G. E. Johnson ◽  
E. A. Sellers

The effects of immunosympathectomy and acclimation to cold on the incorporation of glucose-U-14C into lipids of the interscapular brown adipose tissue, epididymal fat pad, and liver of rats have been investigated. Acclimation to cold was associated with an increase in glucose recovered in the total lipids of brown adipose tissue. These changes in glucose recovery were the same in immunosympathectomized as in intact rats. The brown adipose tissue of the two groups of cold-acclimated rats differed, however, in that this tissue in the immunosympathectomized animals was larger and had more lipid. Suggestions are raised to explain these findings. Neither immunosympathectomy nor cold acclimation produced any changes in white adipose tissue. Immunosympathectomy did not alter the liver's handling of glucose. However, cold-acclimation was associated with an increase in the relative weight of the liver and a decrease in glucose recovery in liver lipids.

1986 ◽  
Vol 250 (2) ◽  
pp. R167-R174
Author(s):  
M. Desautels ◽  
R. A. Dulos

The effects of cold acclimation on brown adipose tissue, heart, and skeletal muscles were evaluated to assess if the increase in metabolic activity associated with chronic exposure to 4 degrees C had any influence on the progression of the syndrome in dystrophic hamsters. Body weight gain was much slower in dystrophic animals kept at 22 degrees C and was unaffected by cold acclimation. Rates of O2 consumption and CO2 production were similar in normal and dystrophic hamsters kept at 22 degrees C, and both were increased in cold-acclimated normal and dystrophic animals. The amount of interscapular brown adipose tissue was about one-half of normal in dystrophic hamsters kept at 22 degrees C. In response to cold acclimation, as in normal hamsters, brown adipose tissue of dystrophic hamsters grew and increased its thermogenin content by more than fourfold. However, the concentration of thermogenin in isolated mitochondria remained unchanged. Heart ventricular hypertrophy was also observed in both normal and dystrophic hamsters after cold acclimation. The number and extent of cardiac necrotic lesions were significantly reduced in cold-acclimated dystrophic animals when compared with age-matched dystrophic hamsters kept at 22 degrees C. Heart calcium content and plasma creatine kinase levels were also reduced in dystrophic hamsters after cold acclimation. However, in soleus muscles the prevalence of centronucleated fibers, an indirect cumulative index of necrosis, as well as the extent of tissue necrosis were not significantly reduced in cold-acclimated dystrophic animals. Thus cold acclimation of dystrophic hamsters appeared to reduce necrosis predominantly in the heart.


1974 ◽  
Vol 52 (1) ◽  
pp. 70-73 ◽  
Author(s):  
M. K. W. Cottle ◽  
W. H. Cottle ◽  
C. W. Nash

Determinations of noradrenaline (NA) content and observations of histochemical fluorescence were carried out on the axillary brown fat pad of ground squirrels Citellus richardsonii kept at two temperatures, 20 °C and 5 °C. For comparison, NA content of hearts and intrathoracic brown adipose tissue were also determined. Like interscapular brown adipose tissue from cold-acclimated rats, the axillary brown fat of cold-acclimated ground squirrels contained a high level of NA. The NA content of the fat pad from ground squirrels living at 20 °C, however, though somewhat lower was not statistically different from that of the fat pad from the cold-acclimated animals. Fine adrenergic nerve fibers were observed between the adipocytes and more intense and extensive networks were present around arterioles. The density of adrenergic innervation appeared similar in the axillary brown fat of the two groups. The NA content of the hearts of ground squirrels living at 5 °C was lower than that for hearts from animals at 20 °C. Intrathoracic brown fat tissue from both groups of animals showed large variation.


1982 ◽  
Vol 60 (5) ◽  
pp. 530-537 ◽  
Author(s):  
Joan Triandafillou ◽  
Cynthia Gwilliam ◽  
Jean Himms-Hagen

The role of thyroid gland in cold-induced growth of brown adipose tissue and in cold-induced adaptive changes in brown adipose tissue mitochondria was investigated. Interscapular brown adipose tissue of thyroidectomized rats maintained at 28 °C was of normal size (protein, cytochrome oxidase content) and its mitochondria were normal, as judged from the level of GDP binding and the polypeptide composition. (GDP binds to a 32 000 dalton polypeptide component of the inner mitochondrial membrane. This component is part of the thermogenic proton conductance pathway. The level of GDP binding is a sensitive indicator of the thermogenic state of the tissue.) Brown adipose tissue mitochondria of thyroidectomized rats exposed to 4 °C for 15 h did not show the usual increase in GDP binding, an indication of a lack of a thermogenic response; the response was restored in thyroxine-treated thyroidectomized animals. In thyroidectomized rats treated with a low maintenance dose of thyroxine (25 μg/kg, s.c., three times per week) and acclimated to cold (4 °C) for 2 weeks, a normal growth of brown adipose (increase in protein and cytochrome oxidase) and normal changes in mitochondria (increase in GDP binding and an increase in the proportion of polypeptides of molecular weight 31 200 – 34 400) occurred. Treatment of intact rats with a large dose of thyroxine (1000 μg/kg, s. c., per day) resulted in a large increase in wet weight, mainly due to lipid accumulation since only small increases in protein and cytochrome oxidase and no change in DNA content occurred; mitochondrial GDP binding was decreased and polypeptide composition unchanged. It is concluded that thyroid hormone exerts a permissive effect on the cold-induced, noradrenaline-mediated, unmasking of GDP-binding sites in brown adipose tissue. The failure of the thyroidectomized rat to survive at 4 °C is probably primarily due to its inability to activate thermogenesis in its brown adipose tissue. Thyroid hormone does not appear to be involved, other than in a permissive way, in long-term cold-induced growth and mitochondrial changes in brown adipose tissue, since these occur normally in the presence of only small amounts of thyroxine in thyroidectomized rats and do not occur in intact rats treated with large amounts of thyroxine.


1988 ◽  
Vol 252 (3) ◽  
pp. 843-849 ◽  
Author(s):  
F J López-Soriano ◽  
J A Fernández-López ◽  
T Mampel ◽  
F Villarroya ◽  
R Iglesias ◽  
...  

The net uptake/release of glucose, lactate and amino acids from the bloodstream by the interscapular brown adipose tissue of control, cold-exposed and cold-acclimated rats was estimated by measurement of arteriovenous differences in their concentrations. In the control animals amino acids contributed little to the overall energetic needs of the tissue; glucose uptake was more than compensated by lactate efflux. Cold-exposure resulted in an enhancement of amino acid utilization and of glucose uptake, with high lactate efflux. There was a net glycine and proline efflux that partly compensated the positive nitrogen balance of the tissue; amino acids accounted for about one-third of the energy supplied by glucose to the tissue. Cold-acclimation resulted in a very high increase in glucose uptake, with a parallel decrease in lactate efflux and amino acid consumption. Branched-chain amino acids, however, were more actively utilized. This was related with a much higher alanine efflux, in addition to that of glycine and proline. It is suggested that most of the glucose used during cold-exposure is returned to the bloodstream as lactate under conditions of active lipid utilization, amino acids contributing their skeletons largely in anaplerotic pathways. On the other hand, cold-acclimation resulted in an important enhancement of glucose utilization, with lowered amino acid oxidation. Amino acids are thus used as metabolic substrates by the brown adipose tissue of rats under conditions of relatively scarce substrate availability, but mainly as anaplerotic substrates, in parallel to glucose. Cold-acclimation results in a shift of the main substrates used in thermogenesis from lipid to glucose, with a much lower need for amino acids.


1982 ◽  
Vol 242 (6) ◽  
pp. E353-E359 ◽  
Author(s):  
L. Bukowiecki ◽  
A. J. Collet ◽  
N. Follea ◽  
G. Guay ◽  
L. Jahjah

Cold acclimation (4 degrees C) and "cafeteria diets" increased the thermic response of rats to catecholamines. This phenomenon was accompanied by six- to eightfold increases of interscapular brown adipose tissue (IBAT) weight, total tissue cytochrome oxidase activity, and total number of brown adipocytes. Quantitative radioautographic experiments using [3H]thymidine disclosed that cold exposure markedly enhanced the mitotic activity in blood capillaries and small-venule endothelial cells, adipose tissue interstitial cells, and preadipocytes rather than in fully differentiated brown adipocytes. IBAT mitotic index increased 70 times over control values after only 2 days of cold exposure. Thereafter, the proliferative activity progressively decreased. IBAT cell composition was modified during cold acclimation as the percentage of interstitial cells and preadipocytes increased over the other cellular types. Because brown adipose tissue is the principal site of norepinephrine-induced thermogenesis in homeothermal animals, it is suggested that brown adipocyte proliferation from precursor cells represents the fundamental phenomenon explaining the increased capacity of cold-acclimated animals to respond calorigenically to catecholamines.


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