An endocrine hypothesis to explain obesity-related lactation insufficiency in breastfeeding mothers.

In this Research Reflection I shall develop and validate the hypothesis that lactation insufficiency in obese breastfeeding mothers has an endocrine explanation. I shall not present data, but I shall review pertinent literature to show that obesity is associated with a partial or sometimes complete failure to initiate and maintain lactation, and critically examine the belief that this is due to psychosocial factors, a failure of prolactin secretion or both. Since progesterone is inhibitory to lactogenesis and oestrogens are inhibitory to milk secretion, I shall then explore the possibility that these steroids are linked to lactation failure, through sequestration of progesterone and aromatization of oestrogen in mammary adipose tissue. I shall conclude by describing experimental approaches in animal models that could be used to test this hypothesis.

Trpc5 deficiency causes hypoprolactinemia and altered function of oscillatory dopamine neurons in the arcuate nucleus.

Dopamine neurons of the hypothalamic arcuate nucleus (ARC) tonically inhibit the release of the protein hormone prolactin from lactotropic cells in the anterior pituitary gland and thus play a central role in prolactin homeostasis of the body. Prolactin, in turn, orchestrates numerous important biological functions such as maternal behavior, reproduction, and sexual arousal. Here, we identify the canonical transient receptor potential channel Trpc5 as an essential requirement for normal function of dopamine ARC neurons and prolactin homeostasis. By analyzing female mice carrying targeted mutations in the Trpc5 gene including a conditional Trpc5 deletion, we show that Trpc5 is required for maintaining highly stereotyped infraslow membrane potential oscillations of dopamine ARC neurons. Trpc5 is also required for eliciting prolactin-evoked tonic plateau potentials in these neurons that are part of a regulatory feedback circuit. Trpc5 mutant females show severe prolactin deficiency or hypoprolactinemia that is associated with irregular reproductive cyclicity, gonadotropin imbalance, and impaired reproductive capabilities. These results reveal a previously unknown role for the cation channel Trpc5 in prolactin homeostasis of female mice and provide strategies to explore the genetic basis of reproductive disorders and other malfunctions associated with defective prolactin regulation in humans.

Breastfeeding a small for gestational age infant, complicated by maternal gestational diabetes: a case report.

BACKGROUND: Small for gestational age (SGA) infants are those born small for their gestational age, with weight below the 10th percentile. Not only do SGA infants suffer growth issues after birth, they have elevated risk for the development of metabolic and cardiovascular diseases later in life. Current research has suggested that in cases of SGA infants, maternal milk and breastfeeding are not affected. The mother of an SGA infant was diagnosed with placental insufficiency and Gestational Diabetes Mellitus (GDM) during her pregnancy. The infant was born term, at 38 weeks 3 days, and SGA. The mother had a low milk supply and her milk composition differed from reference values such that the daily infant intake provided less than 50% of the required energy intake at 3 months. CONCLUSION: In cases of SGA and/or GDM, maternal milk quality and quantity may be compromised. This requires follow-up in order to reduce the disease risk for SGA infants and the corresponding public health implications.

Hormonal and metabolic indicators before and after farrowing in sows affected with postpartum dysgalactia syndrome.

BACKGROUND: Postpartum dysgalactia syndrome (PDS) in sows is difficult to diagnose and the pathogenesis is obscure. Hormonal changes related to the disease are often difficult to distinguish from those found in the normal transition period from gestation to lactation. The study aimed to investigate metabolic and hormonal changes related to PDS with the goal of identifying potential biomarkers in sows suffering from PDS (PDS+). Selected biomarkers were examined by comparing 38 PDS+ sows with 38 PDS negative (PDS-) sows. The sows were sampled every 24 h from 60 h ante partum (a.p.) to 36 h post partum (p.p.). RESULTS: Compared to the baseline (60 to 36 h a.p.), cortisol in serum and saliva and fasting blood glucose concentrations increased in PDS+ as well as PDS- sows. C-peptide decreased relative to the baseline in PDS+ sows, and prolactin and 8-epi prostaglandin F2 alpha (8-epi-PGF2α) decreased in PDS- sows. Concentrations of cortisol in serum and saliva, salivary chromogranin A (CgA), fasting blood glucose, C-peptide, and 8-epi-PGF2α differed significantly between PDS+ and PDS- sows, with levels of cortisol in serum and saliva, salivary CgA, and 8-epi-PGF2α in serum being different in the two groups already before parturition. Concentrations of salivary CgA were significantly lower in PDS- sows than in PDS+ sows during the entire study period. CONCLUSIONS: The results suggest that salivary CgA, cortisol and serum 8-epi-PGF2α may potentially serve as early diagnostic indicators for PDS. The consistently higher salivary CgA concentration in PDS+ sows compared to PDS- sows may indicate that homeostatic disturbances are present between 36 to 60 h before parturition in sows developing PDS. The higher serum and saliva cortisol concentration in PDS+ sows compared to PDS- sows could reflect an early sign of inflammation or stress. The significantly lower C-peptide in PDS+ sows compared to PDS- sows may reflect a lower food intake. Our results contribute to the understanding of the pathogenesis of PDS, and the homeostatic disturbances detected before parturition warrants further investigation. The diagnostic potential of the markers identified in this study should be investigated further in a larger population of sows.

mTOR Inhibition Subdues Milk Disorder Caused by Maternal VLDLR Loss.

It is unknown whether and how very-low density lipoprotein receptors (VLDLRs) impact skeletal homeostasis. Here, we report that maternal and offspring VLDLRs play opposite roles in osteoclastogenesis and bone resorption. VLDLR deletion in the offspring augments osteoclast differentiation by enhancing RANKL signaling, leading to osteoporosis. In contrast, VLDLR deletion in the mother alters milk metabolism, which inhibits osteoclast differentiation and causes osteopetrosis in the offspring. The maternal effects are dominant. VLDLR-null lactating mammary gland exhibits higher mTORC1 signaling and cholesterol biosynthesis. Pharmacological probing reveals that rapamycin, but not statin, treatment of the VLDLR-null mother can prevent both the low bone resorption and our previously described inflammatory fur loss in their offspring. Genetic rescue reveals that maternal mTORC1 attenuation in adipocytes, but not in myeloid cells, prevents offspring osteopetrosis and fur loss. Our studies uncover functions of VLDLR and mTORC1 in lactation and osteoclastogenesis, illuminating key mechanisms and therapeutic insights for bone and metabolic diseases.

Inflammatory mediators in mastitis and lactation insufficiency.

Mastitis is a common inflammatory disease during lactation that causes reduced milk supply. A growing body of evidence challenges the central role of pathogenic bacteria in mastitis, with disease severity associated with markers of inflammation rather than infection. Inflammation in the mammary gland may be triggered by microbe-associated molecular patterns (MAMPs) as well as danger-associated molecular patterns (DAMPs) binding to pattern recognition receptors such as the toll-like receptors (TLRs) on the surface of mammary epithelial cells and local immune cell populations. Activation of the TLR4 signalling pathway and downstream nuclear factor kappa B (NFkB) is critical to mediating local mammary gland inflammation and systemic immune responses in mouse models of mastitis. However, activation of NFkB also induces epithelial cell apoptosis and reduced milk protein synthesis, suggesting that inflammatory mediators activated during mastitis promote partial involution. Perturbed milk flow, maternal stress and genetic predisposition are significant risk factors for mastitis, and could lead to a heightened TLR4-mediated inflammatory response, resulting in increased susceptibility and severity of mastitis disease in the context of low MAMP abundance. Therefore, heightened host inflammatory signalling may act in concert with pathogenic or commensal bacterial species to cause both the inflammation associated with mastitis and lactation insufficiency. Here, we present an alternate paradigm to the widely held notion that breast inflammation is driven principally by infectious bacterial pathogens, and suggest there may be other therapeutic strategies, apart from the currently utilised antimicrobial agents, that could be employed to prevent and treat mastitis in women.

Miz1 deficiency in the mammary gland causes a lactation defect by attenuated Stat5 expression and phosphorylation.

Miz1 is a zinc finger transcription factor with an N-terminal POZ domain. Complexes with Myc, Bcl-6 or Gfi-1 repress expression of genes like Cdkn2b (p15(Ink4)) or Cdkn1a (p21(Cip1)). The role of Miz1 in normal mammary gland development has not been addressed so far. Conditional knockout of the Miz1 POZ domain in luminal cells during pregnancy caused a lactation defect with a transient reduction of glandular tissue, reduced proliferation and attenuated differentiation. This was recapitulated in vitro using mouse mammary gland derived HC11 cells. Further analysis revealed decreased Stat5 activity in Miz1ΔPOZ mammary glands and an attenuated expression of Stat5 targets. Gene expression of the Prolactin receptor (PrlR) and ErbB4, both critical for Stat5 phosphorylation (pStat5) or pStat5 nuclear translocation, was decreased in Miz1ΔPOZ females. Microarray, ChIP-Seq and gene set enrichment analysis revealed a down-regulation of Miz1 target genes being involved in vesicular transport processes. Our data suggest that deranged intracellular transport and localization of PrlR and ErbB4 disrupt the Stat5 signalling pathway in mutant glands and cause the observed lactation phenotype.

Metabolic evaluation of dairy cows submitted to three different strategies to decrease the effects of negative energy balance in early postpartum / Avaliação metabólica de vacas leiteiras submetidas a três estratégias para diminuir os efeitos do balanço energético negativo no pós-parto inicial

In early lactation dairy cattle suffer metabolic alterations caused by negative energy balance, which predisposes to fatty liver and ketosis. The aim of this study was to evaluate the metabolic condition of high yielding dairy cows subjected to three treatments for preventing severe lipomobilization and ketosis in early lactation. Fifty four multiparous Holstein cows yielding >30 L/day were divided into four groups: control (CN= no treatment), glucose precursor (PG= propylene-glycol), hepatic protector (Mp= Mercepton®), and energy supplement with salts of linolenic and linoleic faty acids (Mg-E= Megalac-E®). Treatments were administrated randomly at moment of calving until 8 weeks postpartum. Blood samples were collected on days 1, 7, 14, 21, 28, 35, 42 and 49 postpartum. Body condition score (BCS) was evaluated at the same periods and milk yield was recorded at 2nd, 4th, 5th, 6th, 7th, and 8th weeks of lactation. Concentrations of non-esterified fatty acids (NEFA), albumin, AST, ß-hydroxybutyrate (BHBA), cholesterol, glucose, total protein, urea and triglycerides were analyzed in blood samples. Cut-off points for subclinical ketosis were defined when BHBA >1.4 mmol/L and NEFA >0.7 mmol/L. General occurrence of subclinical ketosis was 24 percent during the period. An ascendant curve of cholesterol and glucose was observed from the 1st to the 8th week of lactation, while any tendency was observed with BHBA and NEFA, although differences among treatments were detected (p<0.05). BCS decreased from a mean of 3.85 at 1st week to 2.53 at 8th week of lactation (p=0.001). Milk yield was higher in the Mg-E group compared with the other treatment groups (p<0.05) Compared with the CN group, the treatments with Mp and PG did not show significant differences in blood biochemistry and milk yield. Cows receiving PG and Mg-E showed higher values of BHBA and NEFA (P<0.05), indicating accentuated lipomobilization. Supplementation with Mg-E also resulted in significant higher concentrations of cholesterol, BHBA, urea, AST and lower values of glycemia. This performance may be explained by the highest milk yield observed with this treatment. Treatments with PG and Mp did not improve milk yield, compared with control cows, but did not show metabolic evidence of ketosis, fat mobilization or fatty liver. These results suggest that treatment with Mg-E improves milk production but induces a higher negative energy balance leading to moderated lipomobilization and ketone bodies production, increasing the risk of fatty liver.

Durante o início da lactação as vacas leiteiras sofrem transtornos metabólicos causados pelo balanço energético negativo, o que predispõe a infiltração gordurosa hepática e cetose. O objetivo deste estudo foi avaliar o status metabólico de vacas leiteiras de alta produção submetidas a três tratamentos para prevenir severa lipomobilização e cetose no início da lactação. Cinquenta e quatro vacas de raça Holandesa multíparas produzindo >30 L/dia foram divididas em quatro grupos: controle (CN= sem tratamento), precursor de glicose (PG= propileno-glicol), protetor hepático (Mp= Mercepton®) e suplementação com sais de ácidos linolênico e linoléico (Mg-E= Megalac-E®). Amostras de sangue foram coletadas nos dias 1, 7, 14, 21, 28, 35, 42 e 49 do pós-parto. A condição corporal foi avaliada nos mesmos períodos e a produção de leite foi registrada nas semanas 2, 4, 5, 6, 7 e 8 de lactação. As concentrações de ácidos graxos não esterificados (AGNE), albumina, AST, ß-hidroxibutirato (BHB), colesterol, glicose, proteína total, uréia e triglicerídeos foram determinadas nas amostras de sangue. Pontos de corte para diagnosticar cetose subclínica foram definidos quando BHB >1,4mmol/L e AGNE >0,7mmol/L. A ocorrência geral de cetose subclínica foi de 24 por cento durante o período. Uma curva ascendente de colesterol e de glicose foi observada desde a 1ª até a 8ª semana de lactação, enquanto que nenhuma tendência foi observada com BHB e AGNE, embora diferenças entre os tratamentos foram detectadas (p<0,05). A condição corporal diminuiu de uma media de 3,85 na 1ª semana até 2,53 na 8ª semana de lactação (p=0,001). A produção de leite foi superior no grupo de Mg-E comparado com os demais tratamentos. Comparado com o grupo CN, os tratamentos de Mp e PG não mostraram diferenças significativas na bioquímica sanguínea nem na produção de leite (p<0,05) As vacas que receberam PG e Mg-E mostraram maiores valores de AGNE, indicando uma acentuada lipomobilização. A suplementação com Mg-E também resultou em maiores concentrações de colesterol, BHB, uréia, AST e menores valores de glicemia. Este resultado pode ser explicado pela maior produção de leite observada com este tratamento. Os tratamentos com PG e Mp não melhoraram a produção de leite, comparados ao grupo CN, mas também não mostraram evidências metabólicas de cetose, alta lipomobilização nem infiltração gordurosa hepática. Os resultados sugerem que o tratamento com Mg-E melhora a produção de leite, mas induz um balance energético negativo maior levando a moderada lipomobilização e produção de corpos cetônicos, aumentando o risco de fígado gorduroso.

Xanthogranulomatous reaction to a ruptured galactocele.

We describe a case of a 34-year-old, healthy, lactating female with a 2-month history of breast pain and an enlarging, tender mass on her right nipple. Her right breast was firm and mildly engorged without mass, warmth or erythema. A tender, yellow nodule was located on the superior aspect of the nipple, obstructing the flow of milk from this portion of the nipple. A biopsy showed epidermal erosion, sheets of cells with massively distended, foamy cytoplasm in the dermis, and a hypertrophied and occluded glandular duct, consistent with reactive squamous metaplasia. Immunostaining for CD68 confirmed the foamy cells were macrophages, and anti-human milk fat globulin-1 (HMFG1) labeled the substance within the macrophages consistent with human breast milk. Therefore, the lesion could be identified as a xanthogranulomatous reaction to a ruptured galactocele.

Reduction of mammary and liver lipogenesis and alteration of milk composition during lactation in rats by hypothyroidism.

OBJECTIVE: The profound impairment in litter growth produced by untreated maternal hypothyroidism (HypoT) may be a consequence of maternal metabolic dysfunctions affecting lactation. In this work we studied the effects of HypoT on mammary and liver lipid metabolism and its consequences on milk quality. DESIGN: We studied the effects of prolonged 6-propyl-2-thiouracil (PTU)-induced HypoT (0.01% PTU in drinking water starting 8 days before mating until sacrifice) on milk macronutrient composition, liver and mammary lipid metabolism and content and serum lipid, and glucose and insulin concentrations in rats on days 7, 15 (L15), and 20 (L20) of lactation. Mammary and hepatic mRNA abundances of lipogenic enzymes were measured using semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) on L15 and L20. MAIN OUTCOME: Milk lactose and triglycerides (TG) were reduced by HypoT, as well as mammary acetyl CoA carboxylase (ACC) activity on L15 and L20, and ACC and lipoprotein lipase (LPL) mRNA on L20. HypoT also decreased hepatic ACC activity on both days, ACC mRNA on L15 and liver [(3)H]H(2)O incorporation to TGs and TG content on L20. HypoT diminished insulinemia, increased serum total lipids, and decreased serum TGs on some or all the days of lactation studied. CONCLUSION: HypoT produces a drastic decrease in milk TGs; the main cause for this seems to be the decreases in liver TG synthesis and in circulating TGs, which, along with reduced mammary uptake of fatty acids caused by decreased LPL expression and possibly diminished mammary lipogenesis, result in an impaired mammary output of TGs to the milk. Thus, the impaired growth of the litters of HypoT mothers can be largely attributed to the low milk quality along with the impaired milk ejection.

Acción del cadmio durante la lactancia sobre el periodonto de rata / Effect of cadmium on rat periodontium during lactation

El cadmio (Cd) afecta la salud de la población, principalmente si habita en regiones industrializadas. En el periodo perinatal, el organismo es particularmente susceptible a la exposición al Cd. Ya que el Cd puede ser excretado en la leche, nuestro objetivo fue estudiar el efecto sobre el periodondo del primer molar superior de rata de la exposición materna durante la lactancia a agua potable conteniendo bajos niveles de Cd (300mg/l CdCl2). Ratas lactantes (21 días de edad) fueron sacrificadas, sus cabezas separadas y fijadas. En cortes histiológicos seriados de 6 mm fueron estimados los siguientes parámetros de las fibras periodontales: volúmenes de núcleo, citoplasma y célula, relación núcleo/citoplasma y densidad numérica. El peso corporal medio fue 34,86g para el control y 18,56g para el grupo tratado. Las fibras periodontales fueron menores y más numerosas y el tejido conjuntivo más abundante. Así el Cd induce desorganización de las fibras periodontales, indicando una acción directa sobre el periodonto, junto con retardo del desarrollo en las crías

Cadmium (Cd) affects the health of people, mainly tose who live in industrialized regions. The organism is particularly susceptible to Cd exposure at perinatal period. As Cd can be excreted into milk our aims was to study the effect on rat maxillary molar periodontium after maternal exposition to drinking water containing low levels of CD (300 mg/l CDCl2) during lactation. Lactent rats (21 day-old) were sacrefied and the heads separated, fixed and serially sectioned. In 6 mm-thick sections were estimated the following periodontal fiber parameters: nucleus cytoplasm and cell volumes, nucleus/cytoplasm ratio and number density. Mean body weight was 34,86g for the control pups and 18,56g for the treated ones. The periodontal fibers were smaller and more numerous and the connective tissue was more abundant. Thus, CD induced periodontal fibers disorganization, indicating a direct action on periodontium, besides retarded debelopment in pups

Breast hypoplasia and breastfeeding: a case history.

Hypoplasia, or glandular insufficiency, of the breasts is an infrequent cause of breastfeeding failure or infant failure to thrive. Early evaluation of the breasts of early identification of infant indicators can enable mothers to breastfeed while providing appropriate supplementation to facilitate satisfactory hydration and growth. A case report is presented of a highly motivated mother with minimal breast tissue who was able to soothe four of her infants at her breasts, supplying some breastmilk, while providing the bulk of their nutritional requirements by other means. At the time of writing she is tandem breastfeeding as well as providing artificial milk by bottle.

Nutritional consequences of chronic maternal conditions during pregnancy and lactation: lupus and diabetes.

Few treated chronic conditions preclude the ability of a mother to conceive. However, consequences of the condition may undermine the pregnancy or aggravate maternal disease. Most chronic conditions require nutritional intervention beyond the normal needs of pregnancy. Insulin-dependent diabetes mellitus (IDDM) and systemic lupus erythematosus (SLE) are two common autoimmune disorders that affect women of childbearing age. Little has been published about the long-term consequences of current medication regimens for SLE and their interactions with either nutrient metabolism or requirements. More information is available on macronutrient dietary needs and metabolism during pregnancy and lactation in women with IDDM, but little is published about the metabolism of other nutrients in this condition. Thus, the nutritional consequences of treating these diseases during pregnancy and lactation must be evaluated continually.

[Use of tryptophan and thyroidin for complex correction of hormonal disorders in experimental hypogalactia in rats]. / Ispol'zovanie triptofana i tireoidina v kachestve kompleksnoi korrektsii gormonal'nykh narushenii pri éksperimental'noi gipogalaktii krys.

The interlinked functioning of the hypothalamo-hypophyseo-breast and hypothalamo-hypophyseo-thyroid systems in experimental hypogalactia (electric stimulation) as well as a possibility of effective correction of neuroendocrine disorders of lactation were studied using tryptophan in combination with microdoses of thyroidin. The hypothalamic and blood concentrations of monoamines (MA) were determined by fluorometry (spectrofluorometers SFM-22, Contron, Switzerland), the blood levels of hormones were determined by a radioimmunoassay. The effect of chronic stress on the monoaminergic hypothalamic system was shown to be based on an increase in the catecholaminergic tone and suppression of serotoninergic tone. It resulted in the suppression of the synthesis and secretion of prolactin, STH, in an elevated blood level of TSH and a considerable reduction of the level of thyroid hormones. The result was weakened secretory function of the breast. Tryptophan and thyroidin administration to rats, subjected to stress, returned to normal function. The investigation brought to light the idea of pathogenesis of hypogalactia, resulting in a new approach to therapy of this pathological condition.

[Hormonal control of lactation].

We studied the mechanism of normal lactation, especially the roles of prolactin (PRL) and oxytocin (OXT) in the initiation of lactation, the lactation in the women complicated with endocrinological disorders, and medical therapies for stimulation and suppression of lactation. The level of serum PRL increases as pregnancy progresses, and reaches to a peak on the day of delivery. Despite high PRL level, milk secretion does not appear during pregnancy, because the sex steroid hormones suppress binding of PRL to the receptor in the mammary gland. The initiation of milk secretion in puerperal women seems to be closely related to an increase in PRL levels induced by adequate suckling. In the mechanism of suckling-induced PRL increase, OXT from posterior pituitary seems to have an important role. Furthermore, the poor response of PRL to suckling was due to insufficient stimulation to the nipples by suckling because the size of nipples were relatively small in these mothers. The other mechanism involved in lactation is suckling-induced OXT secretion. OXT stimulates milk ejection. Anxiety or fear may inhibit the OXT release. We demonstrated that the number of pulsatile release of OXT by nursing was significantly decreased by the psychological stress induced by mental calculation. In the puerperal women with prolactinomas after surgery, the serum PRL level did not increase during pregnancy and milk secretion in puerperium was poor. In the puerperal women with diabetes mellitus, milk secretion was also poor. One of the causes may be related to the low PRL response to suckling stimuli. PRL stimulates milk yield in the mammary gland, but is not commercially available.(ABSTRACT TRUNCATED AT 250 WORDS)

A relationship between neonatal breast size and cord blood testosterone level.

The present study was performed to determine if any hormone measured in cord blood correlates with the size of the neonatal breast or the presence of galactorrhea. A total of 144 term newborn infants were examined. Estradiol (E2), progesterone (P), testosterone (T), and thyrotropin (TSH) were determined by radioimmunoassay (RIA), and prolactin (PRL) was determined by both RIA and biological activity (BA). The female breast (8.5 +/- 2.0 mm) was found to be larger than that of the male (7.8 +/- 2.1 mm, p less than 0.05). The only hormonal difference between sexes was a higher T level in the male infants (8.0 +/- 3.0 nmol per L vs. 5.5 +/- 1.9 nmol per L, p = 0.002). None of the other hormones measured by RIA correlated with the size of the neonatal breast or the presence of galactorrhea. The BA of PRL was widely variable compared to the PRL RIA but also failed to correlate with neonatal breast size or galactorrhea. This study suggests that T might be one factor in determining the size of the neonatal breast.

Prostaglandin F2 alpha and prolactin in experimental hypogalactia in sows.

Peripheral plasma concentrations of 13,14-dihydro-15-keto-prostaglandin F2alpha(PGFM), progesterone, prolactin and oestrone were determined in 20 sows for two days before and three weeks after parturition. Groups of four sows each received one of the following five treatments post partum: 30 ml sterile 0.9 per cent saline solution intrauterinely; ovariectomy and 30 ml saline solution intrauterinely; 10 ml Lugol's iodine plus 20 ml saline solution intrauterinely; ovariectomy and 10 ml Lugol's iodine plus 20 ml saline solution intrauterinely, or progesterone (0.5 mg [kg bodyweight]-1 intramuscularly). Saline solution and iodine were administered every 48 hours, starting immediately after parturition, for one week. Ovariectomy was performed within eight hours of delivery. Progesterone was given every third day for 12 days. Piglet weight gains were used as a reflection of milk yield. In all sows, oestrone values were elevated before parturition, but fell by the end of delivery and were very low during lactation. PGFM concentrations rose during the last two days of pregnancy to reach maximal values at the time of delivery. Plasma progesterone levels declined concomitantly with the rise in PGFM values before parturition. Basal values of progesterone were achieved within 24 hours after delivery in control sows receiving saline treatment. Progesterone values fell immediately after ovariectomy in sows receiving saline or iodine treatment but were slightly elevated for one week in sows that received only intrauterine iodine treatment, suggesting that complete regression of corpora lutea is prevented by suppression of post parturient uterine prostaglandin production. Sows injected with progesterone maintained plasma values of about 5 to 15 nmol litre-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Prolactin concentration in milk and plasma of puerperal women and patients with galactorrhea.

Prolactin (PRL) concentration was estimated in milk and blood of women with various types of galactorrhea (n = 53) and was compared with lactating (n = 17) and normally menstruating women (n = 36). Mean milk (+/- SD) PRL concentration in lactating women (160 +/- 66 micrograms/l) was similar to that of galactorrhea due to pituitary adenoma (149 +/- 87 micrograms/l, n = 24), thyroid dysfunction (193 +/- 72 micrograms/l, n = 8), functional causes (192 +/- 91 micrograms/l, n = 10) or recent pregnancy (198 +/- 44 micrograms/l, n = 2), but higher than that of sex steroid-induced galactorrhea (85 +/- 53 micrograms/l, n = 9). Plasma PRL concentration in lactating women (208 +/- 102 micrograms/l) was higher than in normal control women (14 +/- 5 micrograms/l) and patients with galactorrhea due to thyroid dysfunction (36 +/- 15 micrograms/l), functional causes (16 +/- 8 micrograms/l), drugs (20 +/- 4 micrograms/l), recent pregnancy (22 +/- 3 micrograms/l) or pituitary adenoma (145 +/- 53 micrograms/l). The milk to plasma PRL concentration ratio was 0.8 +/- 0.4 in lactating women and 1.1 +/- 0.7 in patients with adenoma but significantly higher (p = 99% two-sided) in galactorrhea due to thyroid dysfunction (4.4 +/- 2.1), drugs (3.4 +/- 1.1) or functional causes (12.3 +/- 4.3). Bromocriptine administration reduced PRL in both fluids. It is concluded that in women with galactorrhea milk PRL concentration is similar to that of nursing mothers, but plasma levels of this hormone are significantly lower than that of the latter group in all but the pituitary adenoma related galactorrheas.

Unilateral breast dysfunction in lactating Gambian women.

Approximately 3% of lactating women in a rural Gambian village displayed long-term unilateral breast dysfunction as evidenced by abnormal milk composition and virtual cessation of suckling by the infant. This paper presents case histories of four such women studied over two successive lactations. The average breast-milk output of these women did not differ significantly from the mean value for the remainder of the community, indicating that the non-affected breast was usually able to compensate for the dysfunction. This was confirmed by the fact that the child-rearing record of three of the four women was better than the community average. In two of the women the breast which was dysfunctioning in one lactation reverted completely to normal for the next lactation. It is suggested that in such cases the dysfunction is self-perpetuating and may be alleviated by counselling mothers to persevere with feeding from the affected breast.

PIP: Approximately 3% of lactating women in a rural Gambian village displayed longterm unilateral breast dysfunction as evidenced by abnormal milk composition and virtual cessation of suckling by the infant. Case histories of 4 such women, studied over 2 successive lactations, are presented. The average breast milk output of these women did not differ significantly from the mean value for the remainder of the community, indicating that the nonaffected breast was usually able to compensate for the dysfunction. This was confirmed by the fact that the child rearing record of 3 of the 4 women was better than the community average. In 2 of the women, the breast dysfunctioning in 1 lactation reverted completely to normal for the next lactation. It is suggested that in such cases the dysfunction is self-perpetuating and may be alleviated by counseling mothers to persevere with feeding from the affected breast.