[Show abstract][Hide abstract] ABSTRACT: The renal function of rats whose mothers had hypoprolactinemia at the end of lactation was evaluated during development. Lactating Wistar rats were treated with bromocriptine (BRO, 1 mg twice a day, s.c.) or saline on days 19, 20, and 21 of lactation, and their male offspring were followed from weaning until 180 days old. 1 rat from each of the 12 litters/group was evaluated at 2 time points (90 and 180 days). Body and kidney weights, sodium, potassium, and creatinine were measured. Values were considered significant when p<0.05. Adult BRO-treated offspring presented higher body weight (+10%), lower relative renal weight at 90 and 180 days (-9.2% and -15.7%, respectively), glomerulosclerosis, and peritubular fibrosis. At 90 and 180 days, creatinine clearance was lower (-32% and -30%, respectively), whereas serum potassium was higher (+19% and +29%, respectively), but there were no changes in serum sodium. At 180 days, higher proteinuria (+36%) and serum creatinine levels (+20%) were detected. Our data suggest that prolactin inhibition during late lactation programs renal function damage in adult offspring that develops gradually, first affecting the creatinine clearance and potassium serum levels with further development of hyperproteinuria and higher serum creatinine, without affecting sodium. Thus, precocious weaning programs some components of the metabolic syndrome, which can be a risk factor for further development of kidney disease.
Full-text · Article · Aug 2011 · Hormone and Metabolic Research
[Show abstract][Hide abstract] ABSTRACT: Maternal hypoprolactinemia at the end of lactation in rats reduces milk production and is associated with offspring's malnutrition. Since malnutrition during development is also known to have long lasting effects on cognition and emotion, in the present study we tested the hypothesis that maternal hypoprolactinemia, induced by bromocriptine treatment, at the end of the lactating period affects memory/learning, novelty-seeking and anxiety-like behaviors in adult male Wistar rats using, respectively, the radial arm water maze (RAWM), the hole board (HB) arena and the elevated plus-maze (EPM). We also analyzed serum corticosterone and thyroid hormone levels at postnatal day (PN) 21. Lactating dams were treated with bromocriptine (BRO, 1mg twice a day, inhibiting prolactin) or saline from PN19 to 21 (the last 3 days of lactation). BRO offspring had hypercorticosteronemia and hypothyroidism at PN21. In the RAWM, reductions in latency observed in CON rats were initially more accentuated than in BRO ones. By the end of the testing period, latencies became similar between groups. No difference was observed between groups regarding the number of nose-pokes in the HB. In the EPM, BRO rats stayed less time in and had fewer entries into the open-arms than CON ones. This pattern of results indicates that maternal bromocriptine treatment at the end of the lactating period results in poorer memory/learning performance and in higher levels of anxiety-like behavior in the adult offspring, demonstrating that even a relatively short period of malnutrition during development can have long lasting detrimental effects regarding cognition and emotion.
[Show abstract][Hide abstract] ABSTRACT: Maternal hypoprolactinemia at the end of lactation (a precocious weaning model) increases milk leptin transfer and results in overweight, leptin resistance, and secondary hypothyroidism at adulthood. We studied the effects of prolactin (PRL) inhibition during mid-lactation (a partial malnutrition model) on milk leptin transfer, leptinemia, body composition, and thyroid function. Lactating rats were treated with bromocryptine (BRO, 1 mg/twice daily) or saline on days 7, 8, and 9 of lactation. Offspring were sacrificed 10, 21, and 90 days after birth. After treatment, BRO-treated dams showed hypoprolactinemia and hyperleptinemia, and produced less milk with lower levels of lactose and higher milk triglycerides. Milk leptin levels were lower at weaning. Offspring of BRO-treated dams had lower body weight and length as well as less visceral fat during lactation and adulthood. Total fat was also lower at weaning and adult life, whereas total protein was higher at 90 days-old. BRO offspring presented lower serum T4 and TSH at 10 days-old and weaning, respectively. When adults, these rats exhibited hypoleptinemia, lower levels of thyroid hormones, and higher TSH. Early inhibition of PRL therefore leads to offspring malnutrition and affects subsequent growth. Also, inhibition of PRL during lactation predisposes offspring to hypothyroidism; however, when the inhibition occurs during late lactation, the hypothyroidism is secondary, whereas when it is restricted to mid-lactation, the thyroid hypofunction is primary. The programming effect of milk suppression thus depends on the developmental stage of offspring.
No preview · Article · May 2010 · Hormone and Metabolic Research
[Show abstract][Hide abstract] ABSTRACT: Neonatal malnutrition is associated with metabolic syndrome in adulthood. Maternal hypoprolactinaemia at the end of lactation (a precocious weaning model) caused obesity, leptin resistance and hypothyroidism in adult offspring, suggesting an association of prolactin (PRL) and programming of metabolic dysfunctions. Metabolic syndrome pathogenesis is still unclear, but abdominal obesity, higher triglycerides, lower high-density lipoprotein (HDL-c) and insulin resistance have been proposed to be important factors involved. We studied the consequences of maternal hypoprolactinaemia during lactation on parameters associated with metabolic syndrome. Lactating Wistar rats were treated with bromocriptine (BRO, 1 mg twice a day) or saline on days 19, 20 and 21 of lactation and their offspring were followed from weaning until 180 days old. Adult BRO offspring had higher body weight (+10%, P < 0.05), total body fat (+41%, P < 0.05), visceral fat (+20%, P < 0.05), subcutaneous fat (+3 times, P < 0.05) and total body protein (+24%, P < 0.05). BRO group presented hyperglycaemia (+16%, P < 0.05), lower muscle glycogen (−51%, P < 0.05), higher cholesterol (+30%, P < 0.05), higher low-density lipoprotein (LDL-c) (+1.5 times, P < 0.05), higher triglycerides (+49%, P < 0.05), lower HDL-c (−28%, P < 0.05), hyperleptinaemia (+2.9 times, P < 0.05), hypoadiponectinaemia (−16%, P < 0.05) and hypoprolactinaemia (−54%, P < 0.05) as well as higher insulin resistance index (+24%, P < 0.05). Regarding adrenal function, BRO rats showed hypercorticosteronaemia (+46%, P < 0.05) and higher total catecholamine (+37%, P < 0.05). In the hypothalamus, no change was observed in protein expression of the leptin signalling pathway. Thus, neonatal malnutrition induced by maternal PRL inhibition during late lactation programs for obesity, dyslipidaemia and insulin resistance in adult offspring increasing the risk for metabolic syndrome development.
Full-text · Article · Oct 2009 · The Journal of Physiology
[Show abstract][Hide abstract] ABSTRACT: Malnutrition during lactation is associated with hypoprolactinemia and failure in milk production. Adult rats whose mothers were malnourished presented higher body weight and serum tri-iodothyronine (T(3)). Maternal hypoprolactinemia at the end of lactation caused higher body weight in adult life, suggesting an association between maternal prolactin (PRL) level and programming of the offspring's adult body weight. Here, we studied the consequences of the maternal PRL inhibition at the end of lactation by bromocriptine (BRO) injection, a dopaminergic agonist, upon serum TSH and thyroid hormones, thyroid iodide uptake, liver mitochondrial alpha-glycerophosphate dehydrogenase (mGPD), liver and pituitary de-iodinase activities (D1 and/or D2), and in vitro post-TRH TSH release in the adult offspring. Wistar lactating rats were divided into BRO - injected with 1 mg/twice a day, daily for the last 3 days of lactation, and C - control, saline-injected with the same frequency. At 180 days of age, the offspring were injected with (125)I i.p. and after 2 h, they were killed. Adult animals whose mothers were treated with BRO at the end of lactation presented lower serum TSH (-51%), T(3) (-23%), and thyroxine (-21%), lower thyroid (125)I uptake (-41%), liver mGPD (-55%), and pituitary D2 (-51%) activities, without changes in the in vitro post-TRH TSH release. We show that maternal PRL suppression at the end of lactation programs a hypometabolic state in adulthood, in part due to a thyroid hypofunction, caused by a central hypothyroidism, probably due to decreased TRH secretion. We suggest that PRL during lactation can regulate the hypothalamus-pituitary-thyroid axis and programs its function.
Full-text · Article · Jun 2008 · Journal of Endocrinology
[Show abstract][Hide abstract] ABSTRACT: Several authors have shown that secondary hypothyroidism was programed by neonatal thyroxine (T4) treatment. However, the associated changes of body weight (BW) were less studied, especially those related to the body fat proportion. Here, we have evaluated the effect of neonatal thyroxine treatment on BW, fat proportion, serum leptin, and thyroid function of 60-day-old rats. Wistar rats were treated with thyroxine (50 microg/100 g BW, ip) (T) or saline (S), during the first 10 days of life. BW, nose-rump length (NRL), and food consumption were monitored for 60 days, when the animals were sacrificed. Thyroid function was evaluated by thyroid radioiodine uptake (RAIU), serum T3, T4, TSH, and liver mitochondrial alpha-glycerophosphate dehydrogenase (mGPD) and type 1 and 2 deiodinases (D1 and D2) activities, which are thyroid hormone-dependent enzymes. T animals showed lower food intake, BW and NRL, but higher total fat mass (+33%) and serum leptin (+46%). They also showed lower serum T3 (-23%), T4 (-32%), TSH (-36%), RAIU (-29%) and mGPD activity (-22%). Hypothalamic and pituitary D2 activities were higher (+24% and 1.4 fold, respectively), while brown adipose tissue (BAT) D2 and skeletal muscle D1 activities were lower (-30% and -62%, respectively). Thus, neonatal hyperthyroidism programs for a higher fat proportion and hyperleptinemia, which can explain the lower food intake. The TH-dependent enzymes activities changed accordingly, except for the decrease in BAT D2, which may be due the role played by the hyperleptinemia. Finally, the decrease in peripheral deiodination may contribute to a lower me-tabolic rate that may increase the adiposity.
No preview · Article · Feb 2008 · Hormone and Metabolic Research
[Show abstract][Hide abstract] ABSTRACT: Protein malnutrition during neonatal programs for a lower body weight and hyperthyroidism in the adult offspring were analyzed. Liver deiodinase is increased in such animals, contributing to the high serum triiodothyronine (T3) levels. The level of deiodinase activities in other tissues is unknown. We analyzed the effect of maternal protein restriction during lactation on thyroid, skeletal muscle, and pituitary deiodinase activities in the adult offspring. For pituitary evaluation, we studied the in vitro, thyrotropin-releasing hormone (TRH)-stimulated thyroid-stimulating hormone (TSH) secretion. Lactating Wistar rats and their pups were divided into a control (C) group, fed a normal diet (23% protein), and a protein-restricted (PR) group, fed a diet containing 8% protein. At weaning, pups in both groups were fed a normal diet until 180 days old. The pituitary gland was incubated before and after TRH stimulation, and released TSH was measured by radioimmunoassay. Deiodinase activities (D1 and D2) were determined by release of (125)I from [(125)I]reverse triiodothyronine (rT3). Maternal protein malnutrition during lactation programs the adult offspring for lower muscle D2 (-43%, P<0.05) and higher muscle D1 (+83%, P<0.05) activities without changes in thyroidal deiodinase activities, higher pituitary D2 activity (1.5 times, P<0.05), and lower TSH response to in vitro TRH (-56%, P<0.05). The evaluations showed that the lower in vivo TSH detected in adult PR hyperthyroid offspring, programmed by neonatal undernutrition, may be caused by an increment of pituitary deiodination. As described for liver, higher skeletal muscle D1 activity suggests a hyperthyroid status. Our data broaden the knowledge about the adaptive changes to malnutrition during lactation and reinforce the concept of neonatal programming of the thyroid function.
Full-text · Article · Feb 2008 · Experimental Biology and Medicine
[Show abstract][Hide abstract] ABSTRACT: We had previously shown that neonatal leptin treatment programs thyroid function in adulthood. As both thyroid hormones (TH) and leptin increased thermogenesis, it was interesting to evaluate the effect of cold exposure on the thyroid function of neonate rats treated with leptin. Pups were divided into two groups: Lep, injected with leptin (8 mug/100 g/BW, s.c.) for the first 10 days of lactation and control (C), injected with saline. When they were 30 days old, the groups were subdivided into two subgroups: LepC and CC, which were exposed to 8 degrees C for 12 h and compared with C and Lep groups, maintained at 25 +/- 1 degrees C. Serum leptin, TH, and TSH were measured by RIA. Type I liver deiodinase (D1) and mitochondrial alpha-glycerol-3-phosphate dehydrogenase (mGPD) activities were assayed by the release of (125)I from (125)I-reverse and colorimetric method respectively. Leptin receptor (OB-Rb) was evaluated by western blot. Lep group had hyperleptinemia (+22%) and lower free tri-iodothyronine (FT(3); -33%). Cold exposure increased TH both in LepC and CC groups compared with respective controls free thyroxine (FT(4):+63 and +39%; FT(3):+75 and +40%). Liver D1 activity was lower in Lep (-22%) and increased with cold exposure (LepC +51% and CC +22%). The mGPD activity was lower in Lep (-34%) and increased (fourfold) when this group is cold exposed. Hypothalamic and thyroidal OB-Rb receptors were lower in Lep group (-47 and -36% respectively) and they were restored to normal levels after cold exposure. Leptin-programmed rats had higher TH response after cold exposure. OB-Rb had a fast response to cold exposure normalizing the lower levels observed in the leptin-programmed animals and may contribute to the higher TH cold responses.
Full-text · Article · Dec 2007 · Journal of Endocrinology
[Show abstract][Hide abstract] ABSTRACT: Previously we have reported that maternal malnutrition during lactation programmes body weight and thyroid function in the adult offspring. In the present study we evaluated the effect of maternal protein restriction during lactation upon body composition and hormones related to glucose homeostasis in adult rats. During lactation, Wistar lactating rats and their pups were divided into two experimental groups: control (fed a normal diet; 23% protein) and protein-restricted (PR; fed a diet containing 8% protein). At weaning, offspring received a normal diet until they were 180 d old. Body weight (BW) and food intake were monitored. Serum, adrenal glands, visceral fat mass (VFM) and carcasses were collected. PR rats showed lower BW (-13%; P < 0.05), VFM (-33%; P < 0.05), total body fat (-33%; P < 0.05), serum glucose (-7%; P < 0.05), serum insulin (-26%, P < 0.05), homeostasis model assessment index (-20%), but higher total adrenal catecholamine content (+90%; P < 0.05) and serum corticosterone concentration (+51%; P < 0.05). No change was observed in food intake, protein mass or total body water. The lower BW of PR rats is due to a reduction of white fat tissue, probably caused by an increase in lipolysis or impairment of lipogenesis; both effects could be related to higher catecholaminergic status, as well as to hypoinsulinaemia. To conclude, changes in key hormones which control intermediary metabolism are programmed by maternal protein restriction during lactation, resulting in BW alterations in adult rats.
Full-text · Article · Dec 2007 · British Journal Of Nutrition
[Show abstract][Hide abstract] ABSTRACT: Leptin has stimulatory effects on the hypothalamic-pituitary-thyroid axis and on deiodinases activities. Here, we evaluated the effect of leptin injection upon in vivo and in vitro thyroid 125I uptake (RAIU). We designed two experiments: acute leptin (LepA) with a single dose of leptin (8 microg/100 g BW/sc), and chronic leptin (LepC), injected with the same dose of LepA, once a day, for 6 days. In parallel, control groups were saline-injected. For in vivo study, part of the animals were injected with 125I (3700 Bq) and killed after 15 or 120 min. In vivo thyroid RAIU was not changed in LepA animals. However, LepC animals showed higher in vivo thyroid RAIU (15 min:+130% and 120 min:+72%; p<0.05). For in vitro study, the other animals were killed and their thyroids were incubated with 125I. Thyroids explants from LepA and LepC groups presented lower thyroid 125I content (-32% and -29% p<0.05, respectively). The amount of our data suggest that, in vitro, leptin causes a direct inhibition of the rat thyroid RAIU, but in vivo, the effect of leptin was different according to the treatment period, which indicates that other indirect mechanisms are involved in the in vivo leptin chronic stimulation of the thyroid gland.
[Show abstract][Hide abstract] ABSTRACT: Recently, we showed that both maternal malnutrition during lactation and leptin treatment during the neonatal period program thyroid function. In this study we evaluate whether maternal leptin treatment during lactation programs thyroid function of the offspring in the adulthood. The dams were divided into 2 groups: Lep-daily sc single injected with 8 microg/100 g of body weight with recombinant rat leptin during the last 3 days of lactation and control group (C) that received the same volume of saline. The 180 day-old animals received a single i.p. injection of (125)I (2.22x10(4) Bq) and they were killed 2 h after the injection. Triiodothyronine (T3), thyroxine (T4), thyrotropin (TSH) and leptin concentrations were measured by radioimmunoassay. The milk of leptin-treated mothers on the last day of treatment had higher leptin (p<0.05) concentration. The pups of the leptin-treated mothers had at 21 days an unchanged T3, T4 and leptin serum concentrations with higher TSH (p<0.05). The offspring of Lep mothers had at 180 days a higher T3 (p<0.05) with normal thyroid (125)I uptake, T4 and TSH serum concentrations compared to the controls. So, the mother's hyperleptinaemia during lactation programs to a higher T3 serum concentration on the offspring, probably by a higher leptin transfer through the milk.
[Show abstract][Hide abstract] ABSTRACT: Maternal malnutrition during lactation reduces prolactin (PRL) and milk production, alters milk composition, and programs the body weight of the offspring. Our study aimed to evaluate the long-term effects of maternal hypoprolactinemia at the end of lactation on food ingestion, body weight, amount of retroperitoneal white adipose tissue (RPWAT), leptinemia, and anorectic leptin effect in the adult offspring. Lactating rats were treated with bromocriptine (BRO), a PRL inhibitor, 1 mg twice a day, or saline (C - control) for the last 3 days of lactation. The body weight and food intake were monitored, and after sacrifice at 180 days, the RPWAT was weighted. In a second experiment, the anorectic leptin effect was tested on 180-day-old animals. Adult offspring whose mothers were BRO-treated showed higher body weight (10%), higher amount of RPWAT (2 x 3 times), higher total body fat (+39%), and hyperleptinemia (2 x 9 times) when compared with C, although food intake did not alter. After injection of leptin, the food ingestion at 2, 4 and 6 h was unaffected in BRO animals, confirming a resistance to the anorectic effect of leptin. Since the maternal PRL inhibition during lactation programs, a higher body weight with no alteration of food ingestion, we suggest a hypometabolic state. The leptin anorectic resistance can be due to the hyperleptinemia. We suggest that PRL changes during lactation can regulate body weight during adulthood.
Full-text · Article · Mar 2007 · Journal of Endocrinology
[Show abstract][Hide abstract] ABSTRACT: Hormones and malnutrition can imprint several changes in the beginning of life that programs homeostatic changes in the adulthood. We analyzed the thyroid function in 21, 30, 60 and 150 days old animals that were injected with leptin on the first 10 days of life, to determine whether this corresponds to a critical period for the establishment of the hormonal imprinting in the programming of the thyroid function. Pups were divided, within 24 hours of birth, into two groups: Lep group, which was injected once daily with 8 microg/100 g B.W. of recombinant mouse leptin for the first 10 days of lactation, and C-control group that received the same volume of saline. Lep group had higher leptin concentration at days 30 (+6 x , p<0.001) and 150 (+108%, p<0.05) than the controls. These animals had lower serum TT4 (-13%; p<0.05) and TT3 (-17.3%; p<0.002) at 30 days and higher serum TT4 and FT4 concentrations at 150 days (+17.5% and +10%, p<0.05 %, respectively, p<0.05) with lower serum TSH concentrations at 60 (-38.5%, p<0.05) and 150 days (-46%, p<0.05). These animals had also lower hepatic mitochondrial alpha-glycerol-3-phosphate dehydrogenase (mGPDH) activity at 21 (-22.5%; p<0.05), 30 (-50.4%; p<0.05) and 150 days (-40%; p<0.05) than the controls. These data show that the leptin injection in the beginning of lactation cause a hypothyroidism on the offspring as soon as 30 days of age and this alteration may be the imprinted factor for the programming of a higher thyroid function at the adulthood.
No preview · Article · Jan 2007 · Hormone and Metabolic Research
[Show abstract][Hide abstract] ABSTRACT: To understand the role of hormonal changes in the lower food ingestion and body weight in protein-restricted lactating rats as well as the higher serum T (3), higher deiodination, iodide and T (3) milk transfer, we measured maternal serum prolactin, leptin, TSH and corticosterone, which are hormones that could influence those parameters. After birth, dams were separated into: control-fed with a 23 % protein diet (n = 12) and PR (protein-restricted)-fed with an 8 % protein diet (n = 12). At the 4 (th) and 21 (st) day of lactation, half of the animals in each group were sacrificed. PR dams presented hyperleptinemia (day 4: + 20 %; day 21: + 19 %; p < 0.05) and hypoprolactinemia (day 4: - 85 %; day 21: - 92 %; p < 0.05), which could help explain the lower food consumption and body weight in lactating PR rats since leptin is anorexigenic and prolactin is orexigenic. Also, this hyperleptinemia could contribute for the increase in serum T (3) of PR dams, since leptin stimulates T (3) production, especially acting on deiodinases. Serum corticosterone was not different between PR and C groups, and TSH was lower only at the end of lactation. Thus, we suggest that both leptin and prolactin could play an important role in the body weight and thyroid hormone changes observed in protein-malnourished lactating rats.
No preview · Article · May 2006 · Hormone and Metabolic Research
[Show abstract][Hide abstract] ABSTRACT: Malnutrition during lactation reduces milk production and changes pup's leptin serum levels. To test prolactin role in this nutritional state, we evaluated whether prolactin suppression during lactation changes serum leptin in dams, its transfer through the milk, and pup's serum leptin. Lactating rats were treated with bromocryptine (1 mg/twice a day, s.c.) or saline three days before sacrifice (days 2-4 or days 19-21). Food intake and body weight were measured until sacrifice (4th and 21st day). Serum prolactin and leptin were determined by radioimmunoassay. Bromocryptine injected dams had lower serum prolactin and milk production as expected. The mothers presented lower food ingestion (day 21: -25%), lower body weight (day 4: -12%; day 21: -10%), higher serum leptin (day 4: +68%), lower milk leptin on the 4th day (11 times) and higher (8 times) on the 21st day. The offspring of bromocryptine-treated mothers presented lower body weight in both periods of lactation and lower serum leptin on the 4th day (-40%) and higher on the 21st day (+37%) of lactation. We suggest that prolactin, through its effect on leptin secretion into the milk, may play an important role in signalizing maternal nutritional status to the pups.
No preview · Article · May 2005 · Hormone and Metabolic Research
[Show abstract][Hide abstract] ABSTRACT: We investigate whether leptin treatment to lactating rats affects food intake, body weight and leptin serum concentration and its anorectic effect on their adult offspring. Lactating rats were divided into 2 groups: Lep-single injected with recombinant rat leptin (8 microg/100 g of body weight, daily for the last 3 consecutive days of lactation) and control group (C) that received the same volume of saline. After weaning all pups had free access to the control diet, their body weight and food intake were monitored at each 4 days until 180 days of age, when they were tested for its food intake and response to either leptin (0.5 mg/kg body wt, ip) or saline vehicle. The offspring of the leptin-treated dams gained more weight and had higher food intake from day 37 onward (p<0.05), higher amount of retroperitoneal white adipose tissue (RPWAT) (37%, p<0.05) and higher leptin serum concentration (40%, p<0.05) at 180 days of age compared to control group. The food intake at 2, 4, 6 and 24 h was unaffected after acute injection of leptin in these animals, suggesting resistance to the anorectic effect of leptin. The maternal leptin treatment during lactation makes their adult offspring more susceptible to overweight with resistance to the anorectic effect of leptin.
No preview · Article · May 2005 · Regulatory Peptides
[Show abstract][Hide abstract] ABSTRACT: We have previously shown that protein restriction during lactation is associated with changes in iodine secretion into the milk and that a pup's serum leptin concentration was increased at the end of lactation. So, here we evaluate whether leptin treatment during lactation affects iodine transfer through the milk to the pups. Lactating rats were divided into two groups: the leptin (Lep) group, single injected with recombinant rat leptin (8 microg/100g of body weight, daily for 3 consecutive days), and the control (C) group that received the same volume of saline. We studied iodine transfer to the pups through the milk on Days 4, 12 and 21 of lactation. In those days, the dams were separated from their pups for 4 h. Then, the mothers received an injection of 131I (2.22x10(4) Bq ip) and the pups were allowed to nurse for 2 h. The animals were sacrificed 2 h later. Leptin, total serum T3 and total serum T4 concentrations were higher (P<.05) in pups of Lep mothers only on Day 4, suggesting a higher transfer of leptin through the milk at this period, probably with a direct stimulatory effect on thyroid hormone secretion. In other periods, however, even without a detectable increase in a pup's serum leptin concentration, maternal leptin administration increased the pup's thyroid iodine uptake (Day 12, 39%; Day 21, 34%), probably caused by a higher transfer of iodine through the milk, since they had a higher gastric content of 131I on Days 12 (31%) and 21 (128%).
No preview · Article · Mar 2005 · The Journal of Nutritional Biochemistry
[Show abstract][Hide abstract] ABSTRACT: We have shown that protein restriction during lactation is associated with higher levels of serum and milk tri-iodothyronine (T(3)) with lower serum thyroxine (T(4)), suggesting an increased T(4) to T(3) conversion. To investigate this hypothesis, the activity of type 1 (D1) and/or type 2 (D2) iodothyronine deiodinases was evaluated on days 4, 12 and 21 of lactation in several tIssues of dams fed an 8% protein-restricted (PR) diet and controls fed a 23% protein diet. Serum TSH, T(3) and T(4) were measured by radioimmunoassay. Deiodinase activity was determined by the release of (125)I from (125)I-reverse T(3), under specific conditions for D1 or D2. PR dams had a transitory reduction in liver D1 activity (P<0.05) on day 12, and a small increase in thyroid D1 on day 12 followed by a small decrease on day 21. However, thyroid D2 activity was higher than controls (P<0.05) during the whole of the lactation period. Mammary gland D1 and D2 activities were lower on day 4 of lactation in PR dams (P<0.05), and D2 was higher on day 21 (P<0.05). Potentially, a lower conversion of T(3) to di-iodothyronine in the mammary glands of PR dams at the beginning of lactation may serve to provide more T(3) through the milk. Brown adipose tIssue (BAT) D2 activity was higher (P<0.05) in PR dams during all periods of lactation. PR dams showed higher skeletal muscle D1 activity only at the end of lactation, but no changes in D2 activity. Higher pituitary D1 and D2 activities in the PR group (P<0.05) at the end of lactation could have contributed to the lower serum TSH. These data suggest that the higher thyroid and BAT D2 activity during the whole of lactation and skeletal muscle D1 activity at the end of lactation may contribute to the higher serum T(3) in PR dams.
Full-text · Article · May 2003 · Journal of Endocrinology