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Biomedical subjects

D Ricquier

Publications and source records attributed to D Ricquier.

At least 145 records · Page 8Linked to original sources
PubMed1984

Increased level of mRNA for the uncoupling protein in brown adipose tissue of rats during thermogenesis induced by cold exposure or norepinephrine infusion.

We have studied by in vitro translation the mRNA population from rat brown fat in two situations where the thermogenic activity of the tissue is stimulated. Both cold exposure of rats and the presence of pheochromocytoma result in marked alterations among the polypeptides synthesized. Notably, in these two situations there was an increased labeling of polypeptides of the size of the heat-shock proteins and an increased labeling of the 32,000-dalton uncoupling protein of brown fat mitochondria, which is responsible for energy dissipation as heat. Stimulation of the thermogenic activity of brown fat thus results in a high level of mRNA encoding the uncoupling protein. Chronic delivery of norepinephrine mimicked the increase of mRNA for the uncoupling protein observed in animals exposed to cold or bearing pheochromocytoma. Thus, a neuromediator such as norepinephrine is able to trigger the induction of the mRNA encoding the mitochondrial uncoupling protein and is able to stimulate mitochondriogenesis.

Adipose Tissue, Brown↗
PubMed1984

Noradrenaline controls the concentration of the uncoupling protein in brown adipose tissue.

The importance of noradrenaline in the control of the level of the uncoupling protein responsible for the high thermogenic capacity of brown adipose tissue mitochondria was examined. It was observed that chronic infusion of noradrenaline through mini-osmotic pumps increased the mitochondrial concentration of this uncoupling protein to the same extent as chronic exposure to cold.

Adipose Tissue, Brown↗
PubMed1984

Modulation of beta-oxidation and proton conductance pathway of brown adipose tissue in hypo- and hyperinsulinemic states.

The metabolic capacity of interscapular brown adipose tissue of hypoinsulinemic (diabetic) rats is decreased and a reduced beta-oxidative capacity contributes to this metabolic alteration. It was thus of interest to compare, in diabetic and in chronically (8 days) insulin-infused rats, the beta-oxidative capacity and indices of the thermogenic state (GDP-binding and 32 000 Mr protein) in this tissue. Mitochondrial GDP-binding and 32 000 Mr protein were both decreased in diabetic rats compared to appropriate controls and markedly increased as was also the beta-oxidative capacity in hyperinsulinemic rats.

Adipose Tissue↗
PubMed1983

The possible proton translocating activity of the mitochondrial uncoupling protein of brown adipose tissue. Reconstitution studies in liposomes.

Loose coupling of thermogenic mitochondria of brown adipose tissue is related to a high proton (or hydroxyl) conductance of the inner membrane and to the presence of a unique 32 kDa uncoupling protein. Reconstitution experiments of the purified protein in liposomes are reported which suggest that this component could form proton channels in the membrane.

Adenosine Monophosphate↗
PubMed1983

Parallel increase of ascorbic acid and glutathione contents in brown adipose tissue during chronic cold exposure.

Spontaneous lipid peroxidation rate was found unchanged in the brown adipose tissue of rats chronically exposed to cold, although oxidative metabolism, ascorbic acid and poly-unsaturated phospholipid amounts increased. It is suggested that the concomitant increase in glutathione concentration may protect the tissue from a possible peroxidative process.

Adipose Tissue, Brown↗
PubMed1983

Molecular approach to thermogenesis in brown adipose tissue. Cell-free translation of mRNA and characterization of the mitochondrial uncoupling protein.

In order to develop a molecular approach of the thermogenesis mechanism in brown adipose tissue, cell-free translation was performed with mRNA obtained from control or thermoactive brown adipose tissue. Alterations were observed on analysis of the newly synthesized proteins and in particular at the 32,000 dalton level. Experiments using antibodies against the purified characteristic 32,000-dalton uncoupling protein of brown fat mitochondria were carried out. They indicated that the uncoupling protein was synthesized in the reticulocyte lysate with the same apparent molecular weight as the mature form. It is suggested that the development of the thermogenic capacity of brown fat cells is accompanied by an increase in specific mRNA coding for the uncoupling mitochondrial protein and that such a system could be an interesting one for study of mitochondrial membrane biogenesis.

Adipose Tissue, Brown↗
PubMed1983

Fatty acid utilization and purine nucleotide binding in brown adipose tissue of genetically obese (ob/ob) mice.

The activities of the main enzymes involved in fatty acid utilization i.e. palmitoyl CoA synthetase as well as peroxisomal and mitochondrial beta-oxidation were measured in brown adipose tissue homogenates of lean and ob/ob mice kept at 23 degrees C or acclimated at 4 degrees C. The proton conductance pathway, i.e. the number of purine nucleotide (GDP) binding sites and the percentage of 32,000 polypeptide in brown adipose tissue mitochondria were also measured. In the ob/ob mice at 23 degrees C, the specific activities of the palmitoyl CoA synthetase and of the beta-oxidation as well as the number of GDB binding sites were lower than in the lean mice by 26%, 43% and 37%, respectively. The percentage of 32,000 polypeptide, however, was the same in both groups. In the ob/ob mice at 23 degrees C, the lower homogenate beta-oxidation specific activity was due to the fact that the peroxisomal and mitochondrial specific activities were 44% and 37% lower, respectively. Cold acclimation at 4 degrees C was found to cause an increase of the palmitoyl CoA synthetase specific activity, of the palmitoyl CoA synthetase and peroxisomal beta-oxidation total activities and of the number of GDP binding sites, in both lean and ob/ob mice. Cold acclimation increased the percentage of 32,000 polypeptide in the ob/ob mice only.

Adipose Tissue, Brown↗
PubMed1983

An immunological study of the uncoupling protein of brown adipose tissue mitochondria.

1. Ewes were injected with purified 32,000-Mr uncoupling protein from mitochondria of brown adipose tissue of cold-adapted rats in order to raise antibodies. 2. The existence of antibodies in the plasma of ewes and the cross-reactivity of plasmas were demonstrated and studied by 125I-labelled antigen-antibody reaction, double immunodiffusion, the inhibition of GDP binding to the 32,000 Mr protein and by immunohistochemistry. 3. The antibodies raised against the homogeneous protein yielded a single immunoprecipitation band with detergent-solubilized mitochondrial membranes of brown adipose tissue from rat, hamster, guinea-pig, rabbit and with the purified uncoupling protein of these animals. No immunoprecipitation was obtained with the protein purified from brown adipose tissue of term lamb foetus. 4. The GDP-binding activity of the uncoupling protein (isolated or in solubilized membranes) was largely inhibited by the antiserum. 5. The anti-(rat uncoupling protein) could not cross-react with solubilized membranes from liver or muscle, nor with the purified beef heart or rat liver ADP/ATP translocator.

Adipose Tissue, Brown↗
PubMed1983

Development and activation of brown fat in rats with pheochromocytoma PC 12 tumors.

To study the neurohormonal determinism of cellular growth and differentiation and mitochondrial development in brown adipose tissue (BAT), this organ was analyzed in rats bearing uncloned or cloned (PC 12) pheochromocytoma; comparison was made with cold adaptation. Both uncloned and PC 12 tumors induced an enlargement of tissue weight and DNA total content, although smaller than during cold adaptation. The following striking modifications were observed in rats bearing PC 12 tumors: strong vasodilation, increase in protein and phospholipid percentage, alteration of the fatty acid composition of phospholipids, increase in mitochondrial protein, large increase of the GDP binding to isolated mitochondria, and marked rise in specific amount of 32,000-dalton uncoupling protein (ascertained using immunological approach). It is concluded that secretions of PC 12 tumors can induce the same alterations in BAT as does the sympathetic system during cold adaptation of animals. An important contribution of norepinephrine to these effects is evidenced, but a specific function of other trophic factors secreted by PC 12 cells and by sympathetic nerves can be postulated.

Acclimatization↗
PubMed1982

Impairment of trophic response of brown fat to cold in guanethidine-treated rats.

The aim of the present study was to investigate the role of the sympathetic nervous system in the trophic response of brown adipose tissue (BAT) to chronic cold exposure. The hyperplasia and the development of the mitochondria characterizing this response are usually considered as mainly controlled by the sympathetic activity in BAT, but this has never been clearly demonstrated. In the present work rats were sympathectomized by chronic administration of guanethidine and then exposed to cold during two weeks. The treatment induced a strong reduction of the noradrenaline content of BAT. The trophic response of the tissue to cold was largely impaired: no increase of the tissue weight, weak increase in the DNA, protein, and phospholipid content of the tissue. The development of the mitochondria was almost abolished. The increase in the proportion of the 32,000-dalton protein, a protein which regulates heat production by BAT, was suppressed and the GDP-binding to mitochondria, which is an index of BAT thermogenic capacity, was not increased as in normal cold-adapted rats. The ultrastructure of the tissue remained the same as in warm-adapted animals. It is concluded that the sympathetic nervous system plays an essential role in the control of the trophic response of BAT to the cold.

Adaptation, Physiological↗
PubMed1982

Ultrastructural and biochemical characterization of human brown adipose tissue in pheochromocytoma.

The amount and distribution of brown adipose tissue (BAT) in healthy adult human subjects remain uncertain. BAT has been described in patients with pheochromocytoma. This pathological situation was chosen to try to characterize human BAT using both morphological and biochemical criteria. Typical multilocular brown adipocytes were observed; the cytoplasm of these adipocytes was filled with mitochondria with numerous tightly packed cristae, as in rat or hamster BAT. Isolated mitochondria exhibited a loose respiratory coupling sensitive to guanosine diphosphate; the chloride conductance of these mitochondria was reduced by the addition of this nucleotide. It is concluded that in patients with pheochromocytoma, there is a large amount of a tissue around the adrenal glands and kidneys which fullfills the ultrastructural and biochemical criteria for a BAT.

Adipose Tissue, Brown↗
PubMed1981

Effects of hypothyroidism on the brown adipose tissue of adult rats: comparison with the effects of adaptation to cold.

Hypothyroidism was induced in adult rats by oral absorption of methimazole and its effects on brown adipose tissue (BAT) were studied. Hypothyroidism partially mimicked the effects of chronic exposure to cold: BAT weight and its DNA content were increased and the mitochondrial components (proteins, phospholipids) of the tissue were greatly enhanced when expressed per unit of fresh tissue weight. Moreover, hypothyroidism had the same effects as adaptation to cold on the fatty-acid composition of both total and mitochondrial phospholipids. Basal respiratory rate and total cytochrome C oxidase activity of the tissue were also increased. However, the increase in the concentration of the '32,000 mol. wt protein', a polypeptide which regulates the dissipation of heat by BAT, was smaller and non-selective in hypothyroid rats. The amount of this protein was increased per mg tissue, but not per mg mitochondrial proteins, as in rats adapted to cold. Furthermore, in contrast with the large mobilization of the lipid stores in BAT of euthyroid animals, the BAT lipid stores of hypothyroid rats were not mobilized during the first hours of exposure to cold. It may be concluded that (a) hypothyroidism induces several alterations in BAT which are characteristic of an active thermogenic state (this may be because of the response of the organism to the deficiency of thermogenesis induced by hypothyroidism), (b) this potential increase in thermogenic capacity in the BAT of hypothyroid rats has probably a limited physiological role, since thyroid hormones are necessary for the mobilization of the tissue lipids which are the fuel for production of heat and (c) these data provide evidence for a limited role of thyroid hormones in the tropic response of BAT during adaptation to cold.

Adaptation, Physiological↗
PubMed1980

Effects of chronic treatments upon the brown adipose tissue of rats. II. Comparison between the effects of catecholamine injections and cold adaptation.

The role of noradrenaline in the trophic response of brown adipose tissue (BAT) to chronic and cold exposure was studied in young adult rats treated chronically with catecholamines. 2 In young rats, it was difficult to induce a BAT development with this type of treatment. After injection of a beta-agonist (isopropylnoradrenaline) directly upon BAT, a slight hypertrophy of the tissue was observed accompanied by a decrease of its relative protein content. 3 In adult rats, catecholamines were able to induce a growth of BAT and increases of the DNA and protein contents which were as great as in the BAT of cold-exposed rats. 4 Catecholamine treatments did not reproduce the effects of cold exposure on the phospholipids of BAT in either young or adult rats. 5 In the BAT of rats receiving chronically thyroxine and catecholamines, no synergy was observed. Moreover, a chronic treatment by thyroxine induced a slight increase of the DNA content of BAT in rats bred at room temperature, but prevented the marked DNA increase observed in cold-exposed animals.

Adaptation, Physiological↗