jvangard
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I stumbled onto this paper yesterday. It's a couple years old, but it seems no one has referenced it here (hopefully I didn't miss it with my search terms), so I thought it might be of some interest.
I actually have seen T2 bashed on other sites because it doesn't upregulate UCP's and thus thought not to work. This paper indeed says that at least the 3,5 form induces fat loss through an uncoupling process that doesn't require increased UCP's. It also states that at a dose of T2 equivalent to an effective T3 dose in rats, there was no "thyrotoxic" effects after 30 days, ie. no significant change in free T3, free T4, TSH, lean body mass, and thyroid function as evidenced by a TRH challenge. You will note, however that these rats weren't obese in the beginning of the study, but given a very high fat (for rats) diet that can cause them to become obese. In this respect T2 was protective from fat gain. It would be interesting if they had tried this with rats that were already obese from hi fat diet. Interestingly, it is difficult to induce obesity and type II diabetes in normal lab rodents, since they won't overeat...unless given a high fat diet. You'll also note that they cover their butts by saying in essence humans ain't rats.
The FASEB Journal express article 10.1096/fj.05-3977fje. Published online July 12, 2005.
3,5-Diiodo-L-thyronine powerfully reduces adiposity in rats by increasing the burning of fats
Antonia Lanni,* Maria Moreno,†Assunta Lombardi,‡ Pieter de Lange,* Elena Silvestri,† Maurizio Ragni,* Paola Farina,* Gabriella Chieffi Baccari,* Pupah Fallahi,§Alessandro Antonelli,§ and Fernando Goglia†
*Dipartimento di Scienze della Vita, Seconda Università di Napoli, 81100 Caserta;
†Dipartimento di Scienze Biologiche ed Ambientali, Università degli Studi del Sannio, 82100
Benevento; ‡Dipartimento delle Scienze Biologiche Sezione Igiene e Fisiologia, Università degli Studi di Napoli “Federico II,” 80134 Napoli; and §Dipartimento di Medicina Interna, Università degli Studi di Pisa, 56126 Pisa, Italy
ABSTRACT
The effect of thyroid hormones on metabolism has long supported their potential as drugs to stimulate fat reduction, but the concomitant induction of a thyrotoxic state has greatly limited their use. Recent evidence suggests that 3,5-diiodo-L-thyronine (T2), a naturally occurring iodothyronine, stimulates metabolic rate via mechanisms involving the mitochondrial apparatus. We examined whether this effect would result in reduced energy storage. Here, we show that T2 administration to rats receiving a high-fat diet (HFD) reduces both adiposity and body weight gain without inducing thyrotoxicity. Rats receiving HFD + T2 showed (when compared with rats receiving HFD alone) a 13% lower body weight, a 42% higher liver fatty acid oxidation rate, ~50% less fat mass, a complete disappearance of fat from the liver, and significant reductions in the serum triglyceride and cholesterol levels (–52% and –18%, respectively). Thyroid hormones and thyroid-stimulating hormone (TSH) serum levels were not influenced by T2 administration.
The biochemical mechanism underlying the effects of T2 on liver metabolism involves the carnitine palmitoyl-transferase system and mitochondrial uncoupling. If the results hold true for humans, pharmacological administration of T2 might serve to counteract the problems associated with overweight, such as accumulation of lipids in liver and serum, without inducing thyrotoxicity. However, the results reported here do not exclude deleterious effects of T2 on a longer time scale as well as do not show that T2 acts in the same way in humans.
I actually have seen T2 bashed on other sites because it doesn't upregulate UCP's and thus thought not to work. This paper indeed says that at least the 3,5 form induces fat loss through an uncoupling process that doesn't require increased UCP's. It also states that at a dose of T2 equivalent to an effective T3 dose in rats, there was no "thyrotoxic" effects after 30 days, ie. no significant change in free T3, free T4, TSH, lean body mass, and thyroid function as evidenced by a TRH challenge. You will note, however that these rats weren't obese in the beginning of the study, but given a very high fat (for rats) diet that can cause them to become obese. In this respect T2 was protective from fat gain. It would be interesting if they had tried this with rats that were already obese from hi fat diet. Interestingly, it is difficult to induce obesity and type II diabetes in normal lab rodents, since they won't overeat...unless given a high fat diet. You'll also note that they cover their butts by saying in essence humans ain't rats.
The FASEB Journal express article 10.1096/fj.05-3977fje. Published online July 12, 2005.
3,5-Diiodo-L-thyronine powerfully reduces adiposity in rats by increasing the burning of fats
Antonia Lanni,* Maria Moreno,†Assunta Lombardi,‡ Pieter de Lange,* Elena Silvestri,† Maurizio Ragni,* Paola Farina,* Gabriella Chieffi Baccari,* Pupah Fallahi,§Alessandro Antonelli,§ and Fernando Goglia†
*Dipartimento di Scienze della Vita, Seconda Università di Napoli, 81100 Caserta;
†Dipartimento di Scienze Biologiche ed Ambientali, Università degli Studi del Sannio, 82100
Benevento; ‡Dipartimento delle Scienze Biologiche Sezione Igiene e Fisiologia, Università degli Studi di Napoli “Federico II,” 80134 Napoli; and §Dipartimento di Medicina Interna, Università degli Studi di Pisa, 56126 Pisa, Italy
ABSTRACT
The effect of thyroid hormones on metabolism has long supported their potential as drugs to stimulate fat reduction, but the concomitant induction of a thyrotoxic state has greatly limited their use. Recent evidence suggests that 3,5-diiodo-L-thyronine (T2), a naturally occurring iodothyronine, stimulates metabolic rate via mechanisms involving the mitochondrial apparatus. We examined whether this effect would result in reduced energy storage. Here, we show that T2 administration to rats receiving a high-fat diet (HFD) reduces both adiposity and body weight gain without inducing thyrotoxicity. Rats receiving HFD + T2 showed (when compared with rats receiving HFD alone) a 13% lower body weight, a 42% higher liver fatty acid oxidation rate, ~50% less fat mass, a complete disappearance of fat from the liver, and significant reductions in the serum triglyceride and cholesterol levels (–52% and –18%, respectively). Thyroid hormones and thyroid-stimulating hormone (TSH) serum levels were not influenced by T2 administration.
The biochemical mechanism underlying the effects of T2 on liver metabolism involves the carnitine palmitoyl-transferase system and mitochondrial uncoupling. If the results hold true for humans, pharmacological administration of T2 might serve to counteract the problems associated with overweight, such as accumulation of lipids in liver and serum, without inducing thyrotoxicity. However, the results reported here do not exclude deleterious effects of T2 on a longer time scale as well as do not show that T2 acts in the same way in humans.
