scholarly journals A role for thyroid hormones in the regulation of diet-induced thermogenesis in birds

1997 ◽  
Vol 78 (6) ◽  
pp. 963-973 ◽  
Author(s):  
Jean-François Gabarrou ◽  
Claude Duchamp ◽  
John Williams ◽  
Pierre-André Géraert

The possible involvement of thyroid hormones in avian diet-induced thermogenesis (DIT) was investigated in two lines of cockerels divergently selected for high (R-) or low (R+) food efficiency. For a given body weight, R+ cockerels exhibited a higher food intake than R- cockerels (+49 to +76%) and increased DIT (+25%). Plasma thyroxine (T4) levels did not differ between lines whatever the feeding status of the birds. Plasma 3,5,3'-triiodothyronine (T3) level was lower in fasted R+ than in fasted R- cockerels while the opposite was observed after a meal. Iopanic acid injections reduced both plasma T3 concentrations and heat production to the same levels in both lines. Hepatic 5'-deiodinase activity measured with an exogenous sulfhydryl group (dithiothreitol) did not differ between lines, but when the sulfhydryl group was omitted, the activity was higher in R+ than in R- birds (90 ν. 42 pmol T3/min per liver). T3-binding capacity of isolated hepatic nuclei was higher (+76%) in R+ than in R- birds. Long-term or acute pair-feeding of R+ cockerels to the level of R- controls did not alter these results. The present results suggest that T3, mainly originating from peripheral conversion of T4 to T3, is involved in DIT in the R+ line. Availability of endogenous sulfhydryl groups appears to play an important part in the modulation of hepatic deiodinase activity. The higher concentration of nuclear T3 receptors may further increase the effects of the hormone, suggesting a major role of thyroid hormones associated with catecholamines in the stimulation of avian DIT. The underlying thermogenic mechanisms remain to be elucidated.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Igor Lavrov ◽  
Timur Latypov ◽  
Elvira Mukhametova ◽  
Brian Lundstrom ◽  
Paola Sandroni ◽  
...  

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.


2018 ◽  
Vol 115 (14) ◽  
pp. 3698-3703 ◽  
Author(s):  
Xiaofan Jin ◽  
Ingmar H. Riedel-Kruse

Bacterial biofilms represent a promising opportunity for engineering of microbial communities. However, our ability to control spatial structure in biofilms remains limited. Here we engineerEscherichia coliwith a light-activated transcriptional promoter (pDawn) to optically regulate expression of an adhesin gene (Ag43). When illuminated with patterned blue light, long-term viable biofilms with spatial resolution down to 25 μm can be formed on a variety of substrates and inside enclosed culture chambers without the need for surface pretreatment. A biophysical model suggests that the patterning mechanism involves stimulation of transiently surface-adsorbed cells, lending evidence to a previously proposed role of adhesin expression during natural biofilm maturation. Overall, this tool—termed “Biofilm Lithography”—has distinct advantages over existing cell-depositing/patterning methods and provides the ability to grow structured biofilms, with applications toward an improved understanding of natural biofilm communities, as well as the engineering of living biomaterials and bottom–up approaches to microbial consortia design.


CNS Spectrums ◽  
2004 ◽  
Vol 9 (7) ◽  
pp. 523-529 ◽  
Author(s):  
Palmiero Monteleone ◽  
Antonio DiLieto ◽  
Eloisa Castaldo ◽  
Mario Maj

AbstractLeptin is an adipocyte-derived hormone, which is involved predominantly in the long-term regulation of body weight and energy balance by acting as a hunger suppressant signal to the brain. Leptin is also involved in the modulation of reproduction, immune function, physical activity, and some endogenous endocrine axes. Since anorexia nervosa (AN) and bulimia nervosa (BN) are characterized by abnormal eating behaviors, dysregulation of endogenous endocrine axes, alterations of reproductive and immune functions, and increased physical activity, extensive research has been carried out in the last decade in order to ascertain a role of this hormone in the pathophysiology of these syndromes. In this article, we review the available data on leptin physiology in patients with eating disorders. These data support the idea that leptin is not directly involved in the etiology of AN or BN. However, malnutrition-induced alterations in its physiology may contribute to the genesis and/or the maintenance of some clinical manifestations of AN and BN and may have an impact on the prognosis of AN.


Cephalalgia ◽  
1993 ◽  
Vol 13 (2) ◽  
pp. 75-85 ◽  
Author(s):  
Per Kristian Eide ◽  
Kjell Hole

This review shows that the role of 5–hydroxytryptamine (5–HT) in the regulation of nociception depends on the 5–HT receptor subtypes involved and on long-term functional changes in the 5–HT receptors. Stimulation of the 5–HT 1 receptors, as well as of the 5–HT 2 and 5–HT 3 receptors, may reduce nociceptive sensitivity. In addition, activation of 5–HT 2 and 5–HT 3 receptors may also enhance nociceptive sensitivity. Up- or down-regulation of the 5–HT receptors may result in long-lasting changes, plasticity, in the 5–HT systems. Lesioning of 5–HT neurons induces denervation supersensitivity to 5–HT, and prolonged stimulation of 5–HT receptors may produce subsensitivity to 5–HT. In the spinal cord denervation supersensitivity to 5–HT may depend on reduced release of substance P (SP). An increase in the release of SP, on the other hand, may reduce the effects of 5–HT receptor activation. Long-term treatment with antidepressants which are used in clinical pain therapy appears to up-regulate the 5–HT 1 receptors and to down-regulate the 5–HT 2 receptors.


1966 ◽  
Vol 51 (2) ◽  
pp. 315-320 ◽  
Author(s):  
C. M. Goodall ◽  
J. B. Gavin

ABSTRACT Male rats were hypophysectomized at four weeks of age, rested for four weeks, and then were fed a thyroid digest in their drinking water continuously for up to seventy weeks. The digest treatment supplied the equivalent of 1.25μg L-thyroxine per 100 g rat per day approximately. From the body weight curves and radiographic measurements of the skull and mandibles, it was shown that contrary to some previous reports in the literature there was no statistically significant change in the indices of growth or body mass when compared with controls receiving no thyroid treatment. It is suggested that data previously reported by others, indicating a stimulation of growth in hypophysectomized rats by thyroid hormones, may have been derived from animals having minute but still effective pituitary remnants, and somewhat more stringent morphological criteria of hypophysectomy are proposed.


1992 ◽  
Vol 55 (3) ◽  
pp. 670-674 ◽  
Author(s):  
Y Schutz ◽  
A Tremblay ◽  
R L Weinsier ◽  
K M Nelson

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Pavlina Chrysafi ◽  
Nikolaos Perakakis ◽  
Olivia M. Farr ◽  
Konstantinos Stefanakis ◽  
Natia Peradze ◽  
...  

Abstract Based on studies in mice, leptin was expected to decrease body weight in obese individuals. However, the majority of the obese are hyperleptinemic and do not respond to leptin treatment, suggesting the presence of leptin tolerance and questioning the role of leptin as regulator of energy balance in humans. We thus performed detailed novel measurements and analyses of samples and data from our clinical trials biobank to investigate leptin effects on mechanisms of weight regulation in lean normo- and mildly hypo-leptinemic individuals without genetic disorders. We demonstrate that short-term leptin administration alters food intake during refeeding after fasting, whereas long-term leptin treatment reduces fat mass and body weight, and transiently alters circulating free fatty acids in lean mildly hypoleptinemic individuals. Leptin levels before treatment initiation and leptin dose do not predict the observed weight loss in lean individuals suggesting a saturable effect of leptin. In contrast to data from animal studies, leptin treatment does not affect energy expenditure, lipid utilization, SNS activity, heart rate, blood pressure or lean body mass.


2004 ◽  
Vol 380 (2) ◽  
pp. 435-440 ◽  
Author(s):  
Arkaitz CARRACEDO ◽  
Math J. H. GEELEN ◽  
María DIEZ ◽  
Kentaro HANADA ◽  
Manuel GUZMÁN ◽  
...  

Cannabinoids induce apoptosis on glioma cells via stimulation of ceramide synthesis de novo, whereas they do not affect viability of primary astrocytes. In the present study, we show that incubation with Δ9-tetrahydrocannabinol did not induce accumulation of ceramide on astrocytes, although incubation of these cells in a serum-free medium (with or without cannabinoids) led to stimulation of ceramide synthesis de novo and sensitization to oxidative stress. Thus treatment with H2O2 induced apoptosis of 5-day-serum-deprived astrocytes and this effect was abrogated by pharmacological blockade of ceramide synthesis de novo. The sensitizing effect of ceramide accumulation may depend on p38 mitogen-activated protein kinase activation rather than on other ceramide targets. Finally, a protective role of cannabinoids on astrocytes is shown as a long-term incubation with cannabinoids prevented H2O2-induced loss of viability in a CB1 receptor-dependent manner. In summary, our results show that whereas challenge of glioma cells with cannabinoids induces accumulation of de novo-synthesized ceramide and apoptosis, long-term treatment of astrocytes with these compounds does not stimulate this pathway and also abrogates the sensitizing effects of ceramide accumulation.


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