Thermogenic effects of thyrotrophin-releasing hormone and its analogues in the rat

Griffiths, E.C.; Rothwell, Nancy J.; Stock, Michael J.

doi:10.1007/bf01960238

Cited by 17 publications

(11 citation statements)

References 12 publications

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“…Intracranial injection of TRH significantly increased V O 2 , and the increase was maintained for ϳ40 min after injection. It has been reported previously that injection of TRH into the brain increasesVO 2 (14). Therefore, this result demonstrates that the injected samples reached the intracerebral location responsible for the regulation of V O 2 .…”

Section: Effects Of Tgf-␤3 On Spontaneous Motor Activity In Ratssupporting

confidence: 79%

“…Intracranial injection of TRH elevated thermogenesis and V O 2 in rats (14,21). Food restriction before the experiment decreased RER, whereas TRH injection may increase RER.…”

Section: Effects Of Tgf-␤3 On Spontaneous Motor Activity In Ratsmentioning

confidence: 85%

“…3). In this experiment, TRH was injected into the rat brain as a positive control on the basis of the report by Griffiths et al (14) that acute or chronic injection of a TRH analog (RX-77368) and TRH itself stimulated V O 2 in rats (14). They demonstrated that intracranial TRH markedly increased the metabolic rate in rats without any apparent effect on physical activity.…”

Section: Discussionmentioning

confidence: 99%

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Intracranial administration of transforming growth factor-β3 increases fat oxidation in rats

Yamazaki

Arai

Matsumura

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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Yamazaki, Hanae, Masanao Arai, Shigenobu Matsumura, Kazuo Inoue, and Tohru Fushiki. Intracranial administration of transforming growth factor-␤3 increases fat oxidation in rats. Am J Physiol Endocrinol Metab 283: E536-E544, 2002. First published May 28, 2002 10.1152/ ajpendo.00094.2001.-The effects of intracranial transforming growth factor (TGF)-␤3 on spontaneous motor activity and energy metabolism were examined in rats. After injection of TGF-␤3 into the cisterna magna of the rat, spontaneous motor activity decreased significantly for 1 h. The intracranial injection of TGF-␤3 produced an immediate decrease in respiratory exchange ratio (RER). No significant changes were observed in energy expenditure. TGF-␤3 induced a significant increase in total fat oxidation and a decrease in total carbohydrate oxidation. Furthermore, the serum substrates associated with fat metabolism were significantly altered in rats injected with TGF-␤3. Both lipoprotein lipase activity in skeletal muscle and the concentration of serum ketone bodies increased, suggesting that the increase in fat oxidation caused by TGF-␤3 may have occurred in the liver and muscle. Intracranial injection of TGF-␤3 appeared to evoke a switch in the energy substrates accessed in energy expenditure. These results suggest that the release of TGF-␤3 in the brain by exercise is a signal for regulating energy consumption. spontaneous motor activity; respiratory exchange ratio; energy metabolism WE HAVE PREVIOUSLY REPORTED that intracranial administration of cerebrospinal fluid (CSF) from exerciseexhausted rats produced a decrease in spontaneous motor activity, whereas CSF from sedentary rats had no such effect (19).

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Section: Effects Of Tgf-␤3 On Spontaneous Motor Activity In Ratssupporting

confidence: 79%

“…Intracranial injection of TRH elevated thermogenesis and V O 2 in rats (14,21). Food restriction before the experiment decreased RER, whereas TRH injection may increase RER.…”

Section: Effects Of Tgf-␤3 On Spontaneous Motor Activity In Ratsmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

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Intracranial administration of transforming growth factor-β3 increases fat oxidation in rats

Yamazaki

Arai

Matsumura

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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“…The neuronal circuitries involved in the controls of food intake and thermogenesis are numerous and probably to some extent redundant. They comprise neuropeptide Y (NPY), 5,6 thyrotropin-releasinghormone (TRH), 7,8 melanin-concentrating hormone (MCH), 9 proopiomelanocortin (POMC), 10 agoutirelated protein (AGRP), 10 cocaine and amphetamineregulated transcript (CART) 11 systems. These energy balance circuitries also include the corticotropinreleasing hormone (CRH) system, whose role in the regulation of energy balance is presented and discussed in this minireview.…”

Section: Introductionmentioning

confidence: 99%

The corticotropin-releasing hormone system in the regulation of energy balance in obesity

2000

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The view that energy balance is regulated has gained acceptance in recent years. An important role in this regulation is played by brain circuitries involved in the control of energy intake (food intake) and energy expenditure (thermogenesis) that are capable of integrating peripheral signals, produced by perturbations of adipose tissue mass, into messages to effectors of food intake and energy expenditure, so as to prevent substantial variations in the level of energy reserves. More than one neurosystem has been reported to genuinely participate in the regulation of energy balance. Among them is the corticotropin-releasing hormone (CRH) system. This system, with its numerous clusters of brain neurons, its closely related peptide urocortin, its two receptor types and its binding protein, all generally widely distributed throughout the brain, forms a network of neuronal pathways capable of interacting with the circuitries controlling food intake and energy expenditure. In addition, CRH and urocortin's anorectic and thermogenic actions appear to be coordinated to optimize energy losses. Finally, the CRH system seems to demonstrate a certain degree of plasticity in obesity and in response to food deprivation that is consistent with its action on food intake and thermogenesis. The observations have been made that food deprivation and obesity can blunt the expression of the CRH type 2a a receptor in the ventromedial hypothalamic nucleus and can induce the expression of the CRH-binding protein (a CRH-inactivating protein) in brain areas involved in the anorectic and thermogenic actions of CRH.

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“…Chronic TRH and corticosteroid treatment of fetal lambs results in improved lung mechanics and surfactant production (Schellenberg et al 1993), as well as improved cardiovascular adaptation in artificially ventilated, and warmed lambs delivered prematurely by Caesarean section (Stein et al 1994). TRH not only has cardiorespiratory effects but also enhances the thermogenic activity of BAT following acute administration to adult rats (Griffiths et al 1988). We have previously shown that intravenous TRH injection into hypothermic lambs 60-80 min after Caesarean section delivery increases the rate of fat oxidation (Bird et al 1998).…”

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confidence: 95%

Influence of Thyrotrophin‐Releasing Hormone on Thermoregulatory Adaptation after Birth in Near‐Term Lambs Delivered by Caesarean Section

Heasman¹,

Clarke²,

Symonds³

1999

Experimental Physiology

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We investigated the hypothesis that exogenous stimulation with thyrotrophin-releasing hormone (TRH) immediately prior to umbilical cord clamping can improve thermoregulatory adaptation after birth in near-term lambs delivered by Caesarean section. Lambs received an umbilical vein injection of saline +/- TRH (8 microg) prior to cord clamping. The rate of change in colonic temperature and oxygen consumption after birth were not influenced by TRH, but TRH-treated lambs exhibited a greater incidence of shivering compared with controls over the first hour of neonatal life. Two and a half hours after birth, TRH-treated lambs possessed brown adipose tissue (BAT) with a higher thermogenic activity (i.e. GDP binding to mitochondrial protein), but their BAT had a reduced DNA content and they had less hepatic glycogen than control lambs. TRH administration had no effect on iodothyronine 5' deiodinase activity in BAT and liver, or on plasma concentrations of total triiodothyronine, thyroxine, cortisol or free fatty acids. Three TRH-treated but no control lambs, failed to establish continuous breathing, so tissues from these treated lambs together with time-matched controls were sampled 25 min after birth. These 'non-surviving' TRH-treated lambs had very high plasma catecholamine concentrations, but their lung weights were similar to controls. 'Surviving' TRH-treated lambs possessed lungs with less DNA than non-surviving TRH-treated lambs. It is concluded that umbilical vein injection of TRH prior to umbilical cord clamping increases the recruitment of both shivering and non-shivering thermogenesis after birth.

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Thermogenic effects of thyrotrophin-releasing hormone and its analogues in the rat

Cited by 17 publications

References 12 publications

Intracranial administration of transforming growth factor-β3 increases fat oxidation in rats

Intracranial administration of transforming growth factor-β3 increases fat oxidation in rats

The corticotropin-releasing hormone system in the regulation of energy balance in obesity

Influence of Thyrotrophin‐Releasing Hormone on Thermoregulatory Adaptation after Birth in Near‐Term Lambs Delivered by Caesarean Section

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