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MrMakaveli
New member
Esentially extremely bored waiting for my appartment to be ready at school so I did random searching and came across some interesting articles. Scroll to the bottom if you want the easy version of what I'm thinking. I could be wrong but I figured discussion was better than your basic same questions everyday.
Article 1:
Endocrinology. 2004 Aug 5 [Epub ahead of print] Related Articles, Links
Tri-iodothyronine Stimulates Food Intake via the Hypothalamic Ventromedial Nucleus Independent of Changes in Energy Expenditure.
Kong WM, Martin NM, Smith KL, Gardiner JV, Connoley IP, Stephens DA, Dhillo WS, Ghatei MA, Small CJ, Bloom SR.
Department of Metabolic Medicine, Imperial College Faculty of Medicine at Hammersmith Campus, Du Cane Road, London, W12 0NN, U.K.; Department of Physiology, St George's Hospital Medical School, University of London, SW17 0RE, U.K.; Department of Mathematics, Statistics Group, Imperial College, South Kensington Campus, London. SW7 3AZ, U.K.
Increased food intake is characteristic of hyperthyroidism, although this is presumed to compensate for a state of negative energy balance. However, here we show that the thyroid hormone tri-iodothyronine (T3) directly stimulates feeding at the level of the hypothalamus. Peripheral administration of T3 doubled food intake in ad libitum fed rats over 2 h and induced expression of the immediate early gene, Egr-1, in the hypothalamic ventromedial nucleus (VMN), while maintaining plasma fT3 levels within the normal range. T3-induced feeding occurred without altering energy expenditure or locomotion. Injection of T3 directly into the VMN produced a 4-fold increase in food intake in the first hour. The majority of T3 in the brain is reported to be produced by tissue-specific conversion of T4 to T3 by the enzyme type 2 iodothyronine deiodinase (D2). Hypothalamic D2 mRNA expression showed a diurnal variation, with a peak in the nocturnal feeding phase. Hypothalamic D2 mRNA levels also increased following a 12- and 24 h fast, suggesting that local production of T3 may play a role in this T3 feeding circuit. Thus, we propose a novel hypothalamic feeding circuit in which T3, from the peripheral circulation or produced by local conversion, stimulates food intake via the VMN.
PMID: 15297436 [PubMed - as supplied by publisher]
Article 2:
Effect of tri-iodothyronine on leptin release and leptin mRNA accumulation in rat adipose tissue.
Fain JN, Bahouth SW.
Department of Biochemistry, College of Medicine, University of Tennessee, Memphis, TN 38163, USA.
Leptin, the product of the obese gene, is produced by white adipocytes. The release of leptin, as well as leptin mRNA content, was enhanced in adipocytes isolated from hypothyroid rats. The administration of tri-iodothyronine (T3) 8 h before death inhibited leptin release by adipocytes incubated for 6 or 24 h. Direct addition of T3 to pieces of adipose tissue enhanced the loss of leptin mRNA seen over 24 h in the presence of dexamethasone plus the beta3-adrenergic agonist Cl 316,243. In contrast, if pieces of adipose tissue were incubated with dexamethasone plus insulin, enhanced the T3 accumulation of leptin mRNA. These results indicate that T3 enhances net adipocyte leptin mRNA accumulation in a condition that approximates the fed state (presence of insulin) but inhibits leptin mRNA accumulation in a condition that approximates the fasted state (absence of insulin).
Connecting them:
Leptin is an adipocyte-derived blood-borne satiety factor that acts directly on the hypothalamus, thereby regulating food intake and energy expenditure. We have demonstrated that the hypothalamic arcuate nucleus (Arc) is a primary site of the satiety effect of leptin (Neurosci Lett 224:149-152, 1997). To explore the hypothalamic pathway of sympathetic activation of leptin, we examined the effects of a single intravenous or intracerebroventricular injection of recombinant human leptin on catecholamine secretion in rats. We also examined the effects of direct microinjection of leptin into the ventromedial hypothalamus (VMH), Arc, paraventricular nucleus (PVN), and dorsomedial hypothalamus (DMH) in rats. To further assess whether sympathetic activation of leptin is mediated via the VMH, we also examined the effects of a single intravenous injection of leptin in VMH-lesioned rats. A single injection of leptin (0.25-1.0 mg i.v./rat or 0.5-2.0 [micro]g i.c.v./rat) increased plasma norepinephrine (NE) and epinephrine (EPI) concentrations in a dose-dependent manner. Plasma NE and EPI concentrations were increased significantly when leptin was injected directly into the VMH but were unchanged when injected into the Arc, PVN, and DMH. Plasma NE and EPI concentrations were unchanged in VMH-lesioned rats that received a single intravenous injection of leptin. The present study provides evidence that a leptin-induced increase in catecholamine secretion is mediated primarily via the VMH and suggests the presence of distinct hypothalamic pathways mediating the satiety effect and sympathetic activation of leptin. Diabetes 48:1787-1793, 1999
Too much reading? Probably. Here's what it all means (or rather what I'm thinking).
T-3 increases food intake in the VMH independant of metabolic rate. T-3 ALSO inhibits leptin secretion when cutting. So the way around the hunger and subsequent drop in leptlin levels in the VMH? Make the body think it's fed.
Anyone know has read Lyle's bromo book should know that Bromo (or other DA agonists, esp pergolide) trick the body into thinking it's fed when taken with proper timing. So at least in theory if Bromo could do this, it would correct the problem of T-3 inhibition of leptin secretion and possibly improve t-3 fat-loss and *possibly* the rebound.
Could be off. But finding 3 studies that esentially connect was interesting.
Article 1:
Endocrinology. 2004 Aug 5 [Epub ahead of print] Related Articles, Links
Tri-iodothyronine Stimulates Food Intake via the Hypothalamic Ventromedial Nucleus Independent of Changes in Energy Expenditure.
Kong WM, Martin NM, Smith KL, Gardiner JV, Connoley IP, Stephens DA, Dhillo WS, Ghatei MA, Small CJ, Bloom SR.
Department of Metabolic Medicine, Imperial College Faculty of Medicine at Hammersmith Campus, Du Cane Road, London, W12 0NN, U.K.; Department of Physiology, St George's Hospital Medical School, University of London, SW17 0RE, U.K.; Department of Mathematics, Statistics Group, Imperial College, South Kensington Campus, London. SW7 3AZ, U.K.
Increased food intake is characteristic of hyperthyroidism, although this is presumed to compensate for a state of negative energy balance. However, here we show that the thyroid hormone tri-iodothyronine (T3) directly stimulates feeding at the level of the hypothalamus. Peripheral administration of T3 doubled food intake in ad libitum fed rats over 2 h and induced expression of the immediate early gene, Egr-1, in the hypothalamic ventromedial nucleus (VMN), while maintaining plasma fT3 levels within the normal range. T3-induced feeding occurred without altering energy expenditure or locomotion. Injection of T3 directly into the VMN produced a 4-fold increase in food intake in the first hour. The majority of T3 in the brain is reported to be produced by tissue-specific conversion of T4 to T3 by the enzyme type 2 iodothyronine deiodinase (D2). Hypothalamic D2 mRNA expression showed a diurnal variation, with a peak in the nocturnal feeding phase. Hypothalamic D2 mRNA levels also increased following a 12- and 24 h fast, suggesting that local production of T3 may play a role in this T3 feeding circuit. Thus, we propose a novel hypothalamic feeding circuit in which T3, from the peripheral circulation or produced by local conversion, stimulates food intake via the VMN.
PMID: 15297436 [PubMed - as supplied by publisher]
Article 2:
Effect of tri-iodothyronine on leptin release and leptin mRNA accumulation in rat adipose tissue.
Fain JN, Bahouth SW.
Department of Biochemistry, College of Medicine, University of Tennessee, Memphis, TN 38163, USA.
Leptin, the product of the obese gene, is produced by white adipocytes. The release of leptin, as well as leptin mRNA content, was enhanced in adipocytes isolated from hypothyroid rats. The administration of tri-iodothyronine (T3) 8 h before death inhibited leptin release by adipocytes incubated for 6 or 24 h. Direct addition of T3 to pieces of adipose tissue enhanced the loss of leptin mRNA seen over 24 h in the presence of dexamethasone plus the beta3-adrenergic agonist Cl 316,243. In contrast, if pieces of adipose tissue were incubated with dexamethasone plus insulin, enhanced the T3 accumulation of leptin mRNA. These results indicate that T3 enhances net adipocyte leptin mRNA accumulation in a condition that approximates the fed state (presence of insulin) but inhibits leptin mRNA accumulation in a condition that approximates the fasted state (absence of insulin).
Connecting them:
Leptin is an adipocyte-derived blood-borne satiety factor that acts directly on the hypothalamus, thereby regulating food intake and energy expenditure. We have demonstrated that the hypothalamic arcuate nucleus (Arc) is a primary site of the satiety effect of leptin (Neurosci Lett 224:149-152, 1997). To explore the hypothalamic pathway of sympathetic activation of leptin, we examined the effects of a single intravenous or intracerebroventricular injection of recombinant human leptin on catecholamine secretion in rats. We also examined the effects of direct microinjection of leptin into the ventromedial hypothalamus (VMH), Arc, paraventricular nucleus (PVN), and dorsomedial hypothalamus (DMH) in rats. To further assess whether sympathetic activation of leptin is mediated via the VMH, we also examined the effects of a single intravenous injection of leptin in VMH-lesioned rats. A single injection of leptin (0.25-1.0 mg i.v./rat or 0.5-2.0 [micro]g i.c.v./rat) increased plasma norepinephrine (NE) and epinephrine (EPI) concentrations in a dose-dependent manner. Plasma NE and EPI concentrations were increased significantly when leptin was injected directly into the VMH but were unchanged when injected into the Arc, PVN, and DMH. Plasma NE and EPI concentrations were unchanged in VMH-lesioned rats that received a single intravenous injection of leptin. The present study provides evidence that a leptin-induced increase in catecholamine secretion is mediated primarily via the VMH and suggests the presence of distinct hypothalamic pathways mediating the satiety effect and sympathetic activation of leptin. Diabetes 48:1787-1793, 1999
Too much reading? Probably. Here's what it all means (or rather what I'm thinking).
T-3 increases food intake in the VMH independant of metabolic rate. T-3 ALSO inhibits leptin secretion when cutting. So the way around the hunger and subsequent drop in leptlin levels in the VMH? Make the body think it's fed.
Anyone know has read Lyle's bromo book should know that Bromo (or other DA agonists, esp pergolide) trick the body into thinking it's fed when taken with proper timing. So at least in theory if Bromo could do this, it would correct the problem of T-3 inhibition of leptin secretion and possibly improve t-3 fat-loss and *possibly* the rebound.
Could be off. But finding 3 studies that esentially connect was interesting.
