scholarly journals Rapid stimulation of hepatic oxygen consumption by 3,5-di-iodo-l-thyronine

1989 ◽  
Vol 261 (3) ◽  
pp. 945-950 ◽  
Author(s):  
C Horst ◽  
H Rokos ◽  
H J Seitz
Keyword(s):  
Oxygen Consumption ◽  
Thyroid Hormone ◽  
Malic Enzyme ◽  
Mitochondrial Pathway ◽  
Mitochondrial Activity ◽  
O2 Consumption ◽  
Hepatic Oxygen Consumption ◽  
Rapid Stimulation ◽  
Stimulation Of

Tri-iodothyronine (T3) and thyroxine (T4) as well as 3,5-di-iodothyronine (T2) stimulated O2 consumption by isolated perfused livers from hypothyroid rats at a concentration as low as 1 pM by about 30% within 90 min. Application of T2 resulted in a faster stimulation than with application of T3 or T4. Inhibition of iodothyronine monodeiodinase by propylthiouracil, thereby blocking the degradation of T4 to T3 and of T3 to T2, demonstrated that only T2 is the active hormone for the rapid stimulation of hepatic O2 consumption: T3 and T4 lost all of their stimulative activity, whereas T2 was as potent as in the absence of propylthiouracil. Perfusion experiments with thyroid-hormone analogues confirmed the specificity of the T2 effect. The nucleus is unlikely to contribute to the rapid T2 effect, as can be deduced from perfusion experiments with cycloheximide and lack of induction of malic enzyme by T2. In conclusion, a new scheme of regulation of mitochondrial activity is proposed: T2 acts rapidly and directly via a mitochondrial pathway, whereas T3 exerts its long-term action indirectly by induction of specific enzymes.

scholarly journals Thyroid Hormone Stimulation of Autophagy Is Essential for Mitochondrial Biogenesis and Activity in Skeletal Muscle

Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 23-38 ◽  
Author(s):  
Ronny Lesmana ◽  
Rohit A. Sinha ◽  
Brijesh K. Singh ◽  
Jin Zhou ◽  
Kenji Ohba ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Protein Kinase ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Protein ◽  
Adenosine Monophosphate ◽  
Mitochondrial Activity ◽  
Dependent Manner ◽  
In Vivo Models ◽  
Stimulation Of

Abstract Thyroid hormone (TH) and autophagy share similar functions in regulating skeletal muscle growth, regeneration, and differentiation. Although TH recently has been shown to increase autophagy in liver, the regulation and role of autophagy by this hormone in skeletal muscle is not known. Here, using both in vitro and in vivo models, we demonstrated that TH induces autophagy in a dose- and time-dependent manner in skeletal muscle. TH induction of autophagy involved reactive oxygen species (ROS) stimulation of 5′adenosine monophosphate-activated protein kinase (AMPK)-Mammalian target of rapamycin (mTOR)- Unc-51-like kinase 1 (Ulk1) signaling. TH also increased mRNA and protein expression of key autophagy genes, microtubule-associated protein light chain 3 (LC3), Sequestosome 1 (p62), and Ulk1, as well as genes that modulated autophagy and Forkhead box O (FOXO) 1/3a. TH increased mitochondrial protein synthesis and number as well as basal mitochondrial O2 consumption, ATP turnover, and maximal respiratory capacity. Surprisingly, mitochondrial activity and biogenesis were blunted when autophagy was blocked in muscle cells by Autophagy-related gene (Atg)5 short hairpin RNA (shRNA). Induction of ROS and 5′adenosine monophosphate-activated protein kinase (AMPK) by TH played a significant role in the up-regulation of Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PPARGC1A), the key regulator of mitochondrial synthesis. In summary, our findings showed that TH-mediated autophagy was essential for stimulation of mitochondrial biogenesis and activity in skeletal muscle. Moreover, autophagy and mitochondrial biogenesis were coupled in skeletal muscle via TH induction of mitochondrial activity and ROS generation.

scholarly journals The Mechanism of the Calorigenic Action of Thyroid Hormone

1971 ◽  
Vol 57 (6) ◽  
pp. 710-722 ◽  
Author(s):  
Faramarz Ismail-Beigi ◽  
Isidore S. Edelman
Keyword(s):  
Plasma Membrane ◽  
Oxygen Consumption ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Atpase Activity ◽  
Energy Utilization ◽  
Total Oxygen ◽  
Liver Plasma Membrane ◽  
Hormone Stimulation ◽  
Stimulation Of

In an earlier study, we proposed that thyroid hormone stimulation of energy utilization by the Na+ pump mediates the calorigenic response. In this study, the effects of triiodothyronine (T3) on total oxygen consumption (QOO2), the ouabain-sensitive oxygen consumption [QOO2(t)], and NaK-ATPase in liver, kidney, and cerebrum were measured. In liver, ∼90% of the increase in QOO2 produced by T3 in either thyroidectomized or euthyroid rats was attributable to the increase in QOO2(t). In kidney, the increase in QOO2(t) accounted for 29% of the increase in QOO2 in thyroidectomized and 46% of the increase in QOO2 in euthyroid rats. There was no demonstrable effect of T3 in euthyroid rats on QOO2 or QOO2(t) of cerebral slices. The effects of T3 on NaK-ATPase activity in homogenates were as follows: In liver +81% from euthyroid rats and +54% from hypothyroid rats. In kidney, +21% from euthyroid rats and +69% from hypothyroid rats. T3 in euthyroid rats produced no significant changes in NaK-ATPase or Mg-ATPase activity of cerebral homogenates. Liver plasma membrane fractions showed a 69% increase in NaK-ATPase and no significant changes in either Mg-ATPase or 5'-nucleotidase activities after T3 injection. These results indicate that thyroid hormones stimulate NaK-ATPase activity differentially. This effect may account, at least in part, for the calorigenic effects of these hormones.

CHRONIC EFFECTS OF TRIIODOTHYRONINE ON THYROTROPHIN LEVELS IN THYROIDECTOMIZED RATS

1968 ◽  
Vol 57 (1) ◽  
pp. 142-148
Author(s):  
J. L. Bakke ◽  
N. L. Lawrence ◽  
E. Schönbaum
Keyword(s):  
Oxygen Consumption ◽  
Thyroid Hormone ◽  
Pituitary Gland ◽  
Median Eminence ◽  
Thyroid Tissue ◽  
Direct Stimulation ◽  
Chronic Effects ◽  
Small Doses ◽  
Serum Tsh ◽  
Stimulation Of

ABSTRACT In order to study the mechanism of the paradoxical potentiating effect of small doses of thyroid hormone on propylthiouracil goiter growth in rats, serum and pituitary thyrotrophin (TSH) titers were measured after small and larger doses of triiodothyronine (T3) in thyroidectomized rats. A small dose of T3, 4 μg daily, sufficient to maintain normal oxygen consumption, caused elevated pituitary and serum TSH titers when compared to controls. Reduced titers of TSH resulted from a larger dose of T3, 16 μg daily. It is concluded that the goitrogenic action of small doses of thyroid hormone is not limited to an interaction peculiar to propylthiouracil administration but may be the result of direct stimulation of increased synthesis and secretion of TSH by the pituitary gland and is seen even in the absence of thyroid tissue or propylthiouracil. It is hypothesized that small amounts of thyroid hormone are necessary for optimal or maximal synthesis and secretion of TSH. These effects may be mediated directly at the pituitary gland or at a suprapituitary level. It was also found that stalk-median eminence TSH titers were significantly increased in the thyroidectomized rats that received a large dose of T3, as compared to those that received no T3, i. e. the effects were the opposite of those seen in the pituitary gland.

Separation of insulin effects on K content and O2 consumption of frog muscle with cardiac glycosides

1961 ◽  
Vol 200 (6) ◽  
pp. 1320-1326 ◽  
Author(s):  
D. R. H. Gourley
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Cardiac Glycosides ◽  
Oxidation Mechanism ◽  
Frog Muscle ◽  
Transfer System ◽  
O2 Consumption ◽  
Insulin Stimulation ◽  
Lactate Oxidation ◽  
Stimulation Of

Digoxin, deslanoside, or ouabain, in concentrations ranging from 10–9 to 10–4 m, caused a net loss of potassium from isolated intact frog skeletal muscle in the presence of lactate as substrate. The glycosides in concentrations of 10–7 to 10–4 m had little or no effect on oxygen consumption, and the stimulation of oxygen consumption by insulin was not affected by the addition of 1 µm of any of the glycosides. However, the insulin stimulation of potassium uptake by the muscle was completely blocked by digoxin and almost completely blocked by deslanoside. Insulin and ouabain together caused a greater net loss of potassium than did ouabain alone. Although the mechanisms of these effects on muscle potassium by insulin-glycoside combinations are not fully understood, a possible interpretation is that insulin acts on at least two separate sites in skeletal muscle, the potassium transfer system, and the lactate oxidation mechanism, only the first of which is influenced by cardiac glycosides.

Oxygen Consumption in Platelets of Newborn Infants before and after Stimulation by Thrombin.

1976 ◽  
Vol 35 (03) ◽  
pp. 712-716 ◽  
Author(s):  
D. Del Principe ◽  
G Mancuso ◽  
A Menichelli ◽  
G Maretto ◽  
G Sabetta
Keyword(s):  
Oxygen Consumption ◽  
Cord Blood ◽  
Umbilical Cord ◽  
Newborn Infant ◽  
Umbilical Cord Blood ◽  
Newborn Infants ◽  
O2 Consumption ◽  
Adult Control ◽  
Healthy Newborn ◽  
Before And After

SummaryThe authors compared the oxygen consumption in platelets from the umbilical cord blood of 36 healthy newborn infants with that of 27 adult subjects, before and after thrombin addition (1.67 U/ml). Oxygen consumption at rest was 6 mμmol/109/min in adult control platelets and 5.26 in newborn infants. The burst in oxygen consumption after thrombin addition was 26.30 mμmol/109/min in adults and 24.90 in infants. Dinitrophenol did not inhibit the burst of O2 consumption in platelets in 8 out of 10 newborn infants, while the same concentration caused a decrease in 9 out of 10 adult subjects. Deoxyglucose inhibited the burst in O2 consumption in newborn infant and adult platelets by about 50%. KCN at the concentration of 10−4 M completely inhibited basal oxygen consumption but did not completely inhibit the burst after thrombin. At the concentration of 10−3 M, it inhibited both basal O2 consumption and the burst in infants and adult subjects.

Deep brain stimulation of the posterior limb of the internal capsule in the treatment of central poststroke neuropathic pain of the lower limb: case series with long-term follow-up and literature review

2020 ◽  
Vol 133 (3) ◽  
pp. 830-838 ◽  
Author(s):  
Andrea Franzini ◽  
Giuseppe Messina ◽  
Vincenzo Levi ◽  
Antonio D’Ammando ◽  
Roberto Cordella ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Lower Limb ◽  
Internal Capsule ◽  
Posterior Limb ◽  
Vas Score ◽  
The Mean ◽  
Deep Brain ◽  
Stimulation Of

OBJECTIVECentral poststroke neuropathic pain is a debilitating syndrome that is often resistant to medical therapies. Surgical measures include motor cortex stimulation and deep brain stimulation (DBS), which have been used to relieve pain. The aim of this study was to retrospectively assess the safety and long-term efficacy of DBS of the posterior limb of the internal capsule for relieving central poststroke neuropathic pain and associated spasticity affecting the lower limb.METHODSClinical and surgical data were retrospectively collected and analyzed in all patients who had undergone DBS of the posterior limb of the internal capsule to address central poststroke neuropathic pain refractory to conservative measures. In addition, long-term pain intensity and level of satisfaction gained from stimulation were assessed. Pain was evaluated using the visual analog scale (VAS). Information on gait improvement was obtained from medical records, neurological examination, and interview.RESULTSFour patients have undergone the procedure since 2001. No mortality or morbidity related to the surgery was recorded. In three patients, stimulation of the posterior limb of the internal capsule resulted in long-term pain relief; in a fourth patient, the procedure failed to produce any long-lasting positive effect. Two patients obtained a reduction in spasticity and improved motor capability. Before surgery, the mean VAS score was 9 (range 8–10). In the immediate postoperative period and within 1 week after the DBS system had been turned on, the mean VAS score was significantly lower at a mean of 3 (range 0–6). After a mean follow-up of 5.88 years, the mean VAS score was still reduced at 5.5 (range 3–8). The mean percentage of long-term pain reduction was 38.13%.CONCLUSIONSThis series suggests that stimulation of the posterior limb of the internal capsule is safe and effective in treating patients with chronic neuropathic pain affecting the lower limb. The procedure may be a more targeted treatment method than motor cortex stimulation or other neuromodulation techniques in the subset of patients whose pain and spasticity are referred to the lower limbs.

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