scholarly journals Amino acid and glucose uptake by rat brown adipose tissue. Effect of cold-exposure and acclimation

1988 ◽  
Vol 252 (3) ◽  
pp. 843-849 ◽  
Author(s):  
F J López-Soriano ◽  
J A Fernández-López ◽  
T Mampel ◽  
F Villarroya ◽  
R Iglesias ◽  
...  
Keyword(s):  
Amino Acids ◽  
Adipose Tissue ◽  
Amino Acid ◽  
Brown Adipose Tissue ◽  
Glucose Uptake ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Acid Oxidation ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose

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.

Chronic norepinephrine infusion stimulates glucose uptake in white and brown adipose tissues

1994 ◽  
Vol 266 (3) ◽  
pp. R914-R920 ◽  
Author(s):  
X. Liu ◽  
F. Perusse ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Glucose Uptake ◽  
White Adipose Tissue ◽  
Cold Exposure ◽  
Skeletal Muscles ◽  
Interscapular Brown Adipose Tissue ◽  
Peripheral Tissues ◽  
Glucose Levels ◽  
Brown Adipose

Cold exposure activates the sympathetic nervous system and markedly stimulates glucose uptake in rat peripheral tissues [A. L. Vallerand, F. Perusse, and L. J. Bukowiecki. Am. J. Physiol 259 (Regulatory Integrative Comp. Physiol. 28): R1043-R1049, 1990]. To test whether norepinephrine (NE) mimics the effects of cold exposure, we estimated the effects of chronic NE treatment on tissue glucose uptake by determining the glucose metabolic index using the 2-[1,2-3H(N)]deoxy-D-glucose method. NE was administered in conscious rats at various doses (ranging from 1.9 to 25.1 nmol.kg-1.min-1) during 4 days via minipumps implanted subcutaneously. At doses > 10 nmol.kg-1.min-1, NE maximally stimulated glucose uptake in interscapular brown adipose tissue (approximately 50 times above controls) and epididymal white adipose tissue (approximately 3 times above controls). NE infusion (18.8 nmol.kg-1.min-1) increased the circulating levels of NE from 1.1 +/- 0.1 to 19.2 +/- 0.4 nM (P < 0.001), which is in the range of concentrations for the stimulatory effects of NE on glucose uptake in isolated brown adipocytes. At all concentrations tested, NE infusion did not stimulate glucose uptake in the heart and skeletal muscles. NE treatment did not significantly alter plasma insulin or glucose levels but increased the concentration of circulating free fatty acids. The capacity of brown adipose tissue for NE stimulation of glucose uptake (expressed per g of tissue) was much higher than that of white adipose tissue (100 times), various types of white or red skeletal muscles (10-80 times), or the heart (3-4 times).(ABSTRACT TRUNCATED AT 250 WORDS)

Brown adipose tissue hyperplasia: a fundamental mechanism of adaptation to cold and hyperphagia

1982 ◽  
Vol 242 (6) ◽  
pp. E353-E359 ◽  
Author(s):  
L. Bukowiecki ◽  
A. J. Collet ◽  
N. Follea ◽  
G. Guay ◽  
L. Jahjah
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Interstitial Cells ◽  
Brown Adipocyte ◽  
Brown Adipocytes ◽  
Interscapular Brown Adipose Tissue ◽  
Blood Capillaries ◽  
Brown Adipose

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.

scholarly journals Chronic cold exposure induces autophagy to promote fatty acid oxidation, mitochondrial turnover, and thermogenesis in brown adipose tissue

iScience ◽  
2021 ◽  
pp. 102434
Author(s):  
Winifred W. Yau ◽  
Kiraely Adam Wong ◽  
Jin Zhou ◽  
Nivetha Kanakaram Thimmukonda ◽  
Yajun Wu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Fatty Acid Oxidation ◽  
Cold Exposure ◽  
Acid Oxidation ◽  
Brown Adipose ◽  
Mitochondrial Turnover

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
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Relative Weight ◽  
Fat Pad ◽  
Liver Lipids ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Glucose Recovery ◽  
Intact Rats

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.

Catecholamine turnover in S 5B/P1 and Osborne-Mendel rats: response to a high-fat diet

1984 ◽  
Vol 247 (2) ◽  
pp. R290-R295 ◽  
Author(s):  
J. S. Fisler ◽  
T. Yoshida ◽  
G. A. Bray
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
High Fat Diet ◽  
Turnover Rate ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Catecholamine Turnover ◽  
Norepinephrine Turnover ◽  
Brown Adipose

Catecholamine turnover in response to fasting, cold exposure, and a high-fat diet has been measured in the Osborne-Mendel rat, which readily develops obesity when fed a high-fat diet, and the S 5B/P1 rat, which does not. We have tested the hypothesis that this difference in response to diet might be associated with altered rates of norepinephrine or epinephrine turnover. The endogenous norepinephrine concentration in interscapular brown adipose tissue was significantly greater in fasted S 5B/P1 rats than in fasted Osborne-Mendel rats. The fractional norepinephrine turnover rate in interscapular brown adipose tissue of fasted animals was also greater in the S 5B/P1 rat than in the Osborne-Mendel rat. Cold exposure increased the fractional norepinephrine turnover rate in interscapular brown adipose tissue for both strains of rats but increased the fractional norepinephrine turnover rate in the pancreas in only the Osborne-Mendel rats. The turnover of epinephrine and the adrenal concentration of this hormone were not different between the two strains. Normal and high-fat diets were fed to both strains; the Osborne-Mendel rats were pair fed the high-fat diet to prevent excess weight gain. Endogenous concentrations of norepinephrine in interscapular brown adipose tissue was increased by the high-fat diet; the increase was greater in S 5B/P1 rats. The high-fat diet resulted in increased norepinephrine turnover in interscapular brown adipose tissue of the S 5B/P1 rat but not the Osborne-Mendel rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of cold acclimation in dystrophic hamsters: reduction of heart necrosis

1986 ◽  
Vol 250 (2) ◽  
pp. R167-R174
Author(s):  
M. Desautels ◽  
R. A. Dulos
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Ventricular Hypertrophy ◽  
Body Weight Gain ◽  
Calcium Content ◽  
Co2 Production ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Plasma Creatine Kinase

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.

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats

2003 ◽  
Vol 95 (4) ◽  
pp. 1584-1590 ◽  
Author(s):  
Angel A. Zaninovich ◽  
Inés Rebagliati ◽  
Marcela Raíces ◽  
Conrado Ricci ◽  
Karl Hagmüller
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Mitochondrial Respiration ◽  
Mitochondrial Oxygen Consumption ◽  
Normal Body ◽  
Thyroid Ablation ◽  
Brown Adipose

The effects of long-term cold exposure on muscle and liver mitochondrial oxygen consumption in hypothyroid and normal rats were examined. Thyroid ablation was performed after 8-wk acclimation to 4°C. Hypothyroid and normal controls remained in the cold for an additional 8 wk. At the end of 16-wk cold exposure, all hypothyroid rats were alive and normothermic and had normal body weight. At ambient temperature (24°C), thyroid ablation induced a 65% fall in muscle mitochondrial oxygen consumption, which was reversed by thyroxine but not by norepinephrine administration. After cold acclimation was reached, suppression of thyroid function reduced muscle mitochondrial respiration by 30%, but the hypothyroid values remained about threefold higher than those in hypothyroid muscle in the warm. Blockade of β- and α1-adrenergic receptors in both hypothyroid and normal rats produced hypothermia in vivo and a fall in muscle, liver, and brown adipose tissue mitochondria respiration in vitro. In normal rats, cold acclimation enhanced muscle respiration by 35%, in liver 18%, and in brown adipose tissue 450% over values in the warm. The results demonstrate that thyroid hormones, in the presence of norepinephrine, are major determinants of thermogenic activity in muscle and liver of cold-acclimated rats. After thyroid ablation, cold-induced nonshivering thermogenesis replaced 3,5,3′-triiodothyronine-induced thermogenesis, and normal body temperature was maintained.

Cold exposure potentiates the effect of insulin on in vivo glucose uptake

1987 ◽  
Vol 253 (2) ◽  
pp. E179-E186 ◽  
Author(s):  
A. L. Vallerand ◽  
F. Perusse ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Glucose Uptake ◽  
White Adipose Tissue ◽  
Cold Exposure ◽  
Skeletal Muscles ◽  
Insulin Injection ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
Insulin Responses

The effects of cold exposure (48 h at 4 degrees C) and insulin injection (0.5 U/kg iv) on the rates of net 2-[3H]deoxyglucose uptake (Ki) in peripheral tissues were investigated in warm-acclimated rats (25 degrees C). Cold exposure and insulin treatment independently increased Ki values in skeletal muscles (soleus, extensor digitorum longus, and vastus lateralis), heart, white adipose tissue (subcutaneous, gonadal, and retroperitoneal), and brown adipose tissue (P less than 0.01). The effects of cold exposure were particularly evident in brown adipose tissue where the Ki increased greater than 100 times. When the two treatments were combined (insulin injection in cold-exposed rats), it was found that cold exposure synergistically enhanced the maximal insulin responses for glucose uptake in brown adipose tissue, all white adipose tissue depots, and skeletal muscles investigated. The results indicate that cold exposure induces an "insulin-like" effect on Ki that does not appear to be specifically associated with shivering thermogenesis in skeletal muscles, because that effect was observed in all insulin-sensitive tissues. The data also demonstrate that cold exposure significantly potentiates the maximal insulin responses for glucose uptake in the same tissues. This potentialization may result from an enhanced responsiveness of peripheral tissues to insulin, possibly occurring at metabolic steps lying beyond the insulin receptor and an increased tissue blood flow augmenting glucose and insulin availability and thereby amplifying glucose uptake.

Sympathoadrenal system and regulation of thermogenesis

1984 ◽  
Vol 247 (2) ◽  
pp. E181-E189 ◽  
Author(s):  
L. Landsberg ◽  
M. E. Saville ◽  
J. B. Young
Keyword(s):  
Adipose Tissue ◽  
Dietary Intake ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Critical Role ◽  
Interscapular Brown Adipose Tissue ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Adult Humans ◽  
Diet Induced Thermogenesis

The sympathetic nervous system (SNS) plays a critical role in the regulation of mammalian thermogenic responses to cold exposure and dietary intake. Catecholamine-stimulated thermogenesis is mediated by the beta-adrenergic receptor. In the rat brown adipose tissue is the major site of metabolic heat production in response to both cold (nonshivering thermogenesis) and diet (diet-induced thermogenesis). Measurements of norepinephrine turnover rate in interscapular brown adipose tissue of the rat demonstrate increased sympathetic activity in response to both cold exposure and overfeeding. In adult humans, a physiologically significant role for brown adipose tissue has not been established but cannot be excluded. It appears likely that dietary changes in SNS activity are related, at least in part, to the changes in metabolic rate that occur in association with changes in dietary intake.

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