Inpatient and outpatient treatment by specialist infant nutrition centres in Argentina effectively reduced child malnourishment.

AIM: We evaluated the impact of inpatient and outpatient treatment provided by an infant nutrition foundation in Las Heras, Mendoza, Argentina and identified the factors that influenced nutritional recovery. METHODS: This 2010-2018 retrospective study was based on 300 children up to 5 years of age with primary malnutrition, who were treated by an inpatient recovery centre, then an outpatient prevention centre. We analysed the children's height, weight, psychomotor development and living conditions when they were admitted, discharged and had received 1 year of outpatient treatment. There were full data on 241 children and just admission and discharge data for 59. RESULTS: The children's mean age on admission and weight were 14.8 ± 12.4 months and 6.9 ± 2.3 kg and they stayed in hospital for a mean of 59.5 ± 49.7 days. We observed a significant increase in the weight-for-age, height-for-age and weight-for-height z-scores when all three time points were compared (p < 0.001). Psychomotor development improved considerably in all patients after treatment. The factors that negatively influenced nutritional recovery were higher age at admission, suboptimal breastfeeding practices, low birth weight, longer hospital stays, younger maternal age and overcrowded housing. CONCLUSION: Combining inpatient recovery and outpatient preventive treatment was effective for undernourished children in Argentina.

Long-term impact of hypothyroidism during gestation and lactation on the mammary gland.

The functional differentiation of the mammary gland (MG) is fundamental for the prevention of mammary pathologies. This process occurs throughout pregnancy and lactation, making these stages key events for the study of pathologies associated with development and differentiation. Many studies have investigated the link between mammary pathologies and thyroid diseases, but most have ignored the role of thyroid hormone (TH) in the functional differentiation of the MG. In this work, we show the long-term impact of hypothyroidism in an animal model whose lactogenic differentiation occurred at low TH levels. We evaluated the ability of the MG to respond to hormonal control and regulate cell cycle progression. We found that a deficit in TH throughout pregnancy and lactation induces a long-term decrease in Rb phosphorylation, increases p53, p21, Cyclin D1 and Ki67 expression, reduces progesterone receptor expression, and induces nonmalignant lesions in mammary tissue. This paper shows the importance of TH level control during mammary differentiation and its long-term impact on mammary function.

Salvage Radical Prostatectomy in Nonmetastatic Castration-Resistant Prostate Cancer.

OBJECTIVE: To analyze the perioperatory and short-oncological outcomes in 5 cases with CRPC M0 developed after pRT that underwent salvage laparoscopic RP (sLRP) and review the current evidence. MATERIAL AND METHODS: Perioperatory and oncological outcomes were prospectively analyzed. Inclusion criteria were patients that had received pRT and posteriorly presented with CRPC M0 in standard imagines and positron emission tomography MRI coline. Evidence was reviewed in PUBMED database. RESULTS: No surgical complications and blood transfusion were reported. Two patients required an endoscopic urethrotomy due to bladder neck contracture (Clavien IIIb). Final pathological findings were T3 or more, multifocal with 3 positive surgical margins. Four patients reach undetectable PSA after surgery except one that continuous under ADT without disease progression. After 12 months follow-up, 4 patients persist with undetectable PSA and one with stable disease under ADT. Current evidence demonstrated that CRPC M0 treated with open, laparoscopic or robotic RP a biochemical recurrence of 68.7% as a hormone-sensitive PC; however, 17.4% were disease-free after 4 years of follow-up. CONCLUSION: Our serie, 4 cases are disease free after 12 months follow-up. Current evidence is a retrospective and multicenter experience with few cases and intermediate oncological follow-up. More cases with longer follow-up and better evidence are required to opt for this treatment as a first line.

The epigenetic role of breastfeeding in mammary differentiation.

Maternal milk consumption can cause changes in the mammary epithelium of the offspring that result in the expression of molecules involved in the induction of differentiation, reducing the risk of developing mammary cancer later in life. We previously showed that animals that maintained a higher intake of maternal milk had a lower incidence of mammary cancer. In the present study, we evaluated one of the possible mechanisms by which the consumption of maternal milk could modify the susceptibility to mammary carcinogenesis. We used Sprague Dawley rats reared in litters of 3 (L3), 8 (L8), or 12 (L12) pups per mother in order to generate a differential consumption of milk. Whole mounts of mammary glands were performed to analyze the changes in morphology. Using real-time polymerase chain reaction (PCR), we analyzed the expression of mammary Pinc, Tbx3, Stat6, and Gata3 genes. We use the real-time methylation-specific polymerase chain reaction method to assess the methylation status of Stat6 and Gata3 CpG sites. Our findings show an increase in the size of the epithelial tree and a smaller number of ducts called terminal end buds in L3 vs. L12. We observed an increased expression of mRNA of Stat6, Gata3, Tbx3, and a lower expression of Pinc in L3 with respect to L12. Stat6 and Gata3 are more methylated in the CpG islands of the promoter analyzed in L12 vs. L3. In conclusion, the increased consumption of maternal milk during the postnatal stage generates epigenetic and morphological changes associated with the differentiation of the mammary gland.

Human renal adipose tissue from normal and tumor kidney: its influence on renal cell carcinoma.

Tumor cells can interact with neighboring adipose tissue. We evaluated components present in human adipose explants from normal (hRAN) and kidney cancer (hRAT) tissue, and we evaluated the effects of conditioned media (CMs) from hRAN and hRAT on proliferation, adhesion and migration of tumor and non-tumor human renal epithelial cell lines. In addition, we evaluated the expression of AdipoR1, ObR, CD44, vimentin, pERK and pPI3K on cell lines incubated with CMs. hRAN were obtained from healthy operated donors, and hRAT from patients who underwent a nephrectomy. hRAT showed increased levels of versican, leptin and ObR; and decreased levels of perilipin, adiponectin and AdipoR1, compared to hRAN. Cell lines showed a significant decrease in cell adhesion and increase in cell migration after incubation with hRAT-CMs vs. hRAN- or control-CMs. Surprisingly, HK-2, 786-O and ACHN cells showed a significant decrease in cell migration after incubation with hRAN-CMs vs. control-CMs. No difference in proliferation of cell lines was found after 24 or 48 h of treatment with CMs. AdipoR1 in ACHN and Caki-1 cells decreased significantly after incubation with hRAT-CMs vs. hRAN-CMs and control-CMs. ObR and CD44 increased in tumor line cells, and vimentin increased in non-tumor cells, after incubation with hRAT-CMs vs. hRAN-CMs and control-CMs. We observed an increase in the expression of pERK and pPI3K in HK-2, 786-O and ACHN, incubated with hRAT-CMs. In conclusion, results showed that adipose microenvironment can regulate the behavior of tumor and non tumor human renal epithelial cells.

Estradiol and progesterone regulate proliferation and apoptosis in colon cancer.

Epidemiological studies describe estrogens as protectors in the development of colon cancer in postmenopausal women treated with hormone replacement therapy. However, the role of progesterone in colon cancer has been minimally studied and the results are controversial. For the above, the objective of this work was to determine the hormonal regulation exerted by natural ovarian steroids on proliferation and apoptosis in an experimental model of colon cancer in ovariectomized rats treated with 17-beta estradiol and progesterone. Sprague-Dawley rats were exposed to the carcinogen 1,2-dimethylhydrazine to induce colon tumors. Thirty days later, the rats were ovariectomized and treated with estradiol (60 µg/kg), progesterone (10 mg/kg), estradiol plus progesterone (60 µg/kg and 10 mg/kg) or vehicle. We observed no significant differences in colon cancer incidence and tumor multiplicity between the groups. Nevertheless, we observed a decrease in PCNA expression and a greater number of apoptotic index, higher expression of caspase 3, cleaved PARP and cleaved caspase 8 in tumors, confirming the activation of the extrinsic pathway of apoptosis by the combined treatment. In addition, we observed a higher expression of estrogen receptor beta in these tumors. We conclude that the action of both hormones, estradiol and progesterone, is necessary to reduce proliferation and increase apoptosis in colon tumors, probably through estrogen receptor beta activation.

Human renal adipose tissue induces the invasion and progression of renal cell carcinoma.

We evaluated the effects of conditioned media (CMs) of human adipose tissue from renal cell carcinoma located near the tumor (hRATnT) or farther away from the tumor (hRATfT), on proliferation, adhesion and migration of tumor (786-O and ACHN) and non-tumor (HK-2) human renal epithelial cell lines. Human adipose tissues were obtained from patients with renal cell carcinoma (RCC) and CMs from hRATnT and hRATfT incubation. Proliferation, adhesion and migration were quantified in 786-O, ACHN and HK-2 cell lines incubated with hRATnT-, hRATfT- or control-CMs. We evaluated versican, adiponectin and leptin expression in CMs from hRATnT and hRATfT. We evaluated AdipoR1/2, ObR, pERK, pAkt y pPI3K expression on cell lines incubated with CMs. No differences in proliferation of cell lines was found after 24 h of treatment with CMs. All cell lines showed a significant decrease in cell adhesion and increase in cell migration after incubation with hRATnT-CMs vs. hRATfT- or control-CMs. hRATnT-CMs showed increased levels of versican and leptin, compared to hRATfT-CMs. AdipoR2 in 786-O and ACHN cells decreased significantly after incubation with hRATfT- and hRATnT-CMs vs. control-CMs. We observed a decrease in the expression of pAkt in HK-2, 786-O and ACHN incubated with hRATnT-CMs. This result could partially explain the observed changes in migration and cell adhesion. We conclude that hRATnT released factors, such as leptin and versican, could enhance the invasive potential of renal epithelial cell lines and could modulate the progression of the disease.

Human breast adipose tissue: characterization of factors that change during tumor progression in human breast cancer.

BACKGROUND: Adipose microenvironment is involved in signaling pathways that influence breast cancer. We aim to characterize factors that are modified: 1) in tumor and non tumor human breast epithelial cell lines when incubated with conditioned media (CMs) from human breast cancer adipose tissue explants (hATT) or normal breast adipose tissue explants (hATN); 2) in hATN-CMs vs hATT-CMs; 3) in the tumor associated adipocytes vs. non tumor associated adipocytes. METHODS: We used hATN or hATT- CMs on tumor and non-tumor breast cancer cell lines. We evaluated changes in versican, CD44, ADAMTS1 and Adipo R1 expression on cell lines or in the different CMs. In addition we evaluated changes in the morphology and expression of these factors in slices of the different adipose tissues. The statistical significance between different experimental conditions was evaluated by one-way ANOVA. Tukey's post-hoc tests were performed within each individual treatment. RESULTS: hATT-CMs increase versican, CD44, ADAMTS1 and Adipo R1 expression in breast cancer epithelial cells. Furthermore, hATT-CMs present higher levels of versican expression compared to hATN-CMs. In addition, we observed a loss of effect in cellular migration when we pre-incubated hATT-CMs with chondroitinase ABC, which cleaves GAGs chains bound to the versican core protein, thus losing the ability to bind to CD44. Adipocytes associated with the invasive front are reduced in size compared to adipocytes that are farther away. Also, hATT adipocytes express significantly higher amounts of versican, CD44 and Adipo R1, and significantly lower amounts of adiponectin and perilipin, unlike hATN adipocytes. CONCLUSIONS: We conclude that hATT secrete a different set of proteins compared to hATN. Furthermore, versican, a proteoglycan that is overexpressed in hATT-CMs compared to hATN-CMs, might be involved in the tumorogenic behavior observed in both cell lines employed. In addition, we may conclude that adipocytes from the tumor microenvironment show a less differentiated state than adipocytes from normal microenvironment. This would indicate a loss of normal functions in mature adipocytes (such as energy storage), in support of others that might favor tumor growth.

Effects of parity and serum prolactin levels on the incidence and regression of DMBA-induced tumors in OFA hr/hr rats.

Prolactin (PRL) is a key player in the development of mammary cancer. We studied the effects of parity or hyperprolactinemia on mammary carcinogenesis in OFA hr/hr treated with 7,12-dimethylbenzanthracene. They were divided into three groups: nulliparous (Null), primiparous (PL, after pregnancy and lactation), and hyperprolactinemic rats (I, implanted in the arcuate nucleus with 17ß-estradiol). The tumor incidence was similar in the three groups. However, a higher percentage of regressing tumors was evident in the PL group. Serum PRL, mammary development, and mammary ß-casein content were higher in I rats compared to Null. The expression of hormone receptors was similar in the different groups. However, mammary tissue from PL rats bearing tumors had increased expression of PRL and estrogen alpha receptors compared to rats free of tumors. Our results suggest that serum PRL levels do not have relevance on the incidence of tumors, probably because the low levels of PRL in OFA rats are not further decreased by PL like in other strains. However, supraphysiological levels of PRL affect carcinogenesis. PL induces regression of the tumors due to the differentiation produced on the mammary cells. Alterations in the expression of hormonal receptors may be involved in progression and regression of tumors.

Experimental hypothyroidism increases apoptosis in dimethylbenzanthracene-induced mammary tumors.

Epidemiological and in vitro data have not provided conclusive evidence concerning the involvement of thyroid hormones (THs) on mammary carcinogenesis. We used an in vivo model to assess the relationship between THs, adipose tissue and breast cancer development. Female Sprague­Dawley rats were treated with a dose of 7,12-dimethylbenz(a)anthracene (15 mg/rat) at 55 days of age and were then divided into four experimental groups: hypothyroid rats (HypoT, 0.01% 6-N-propyl-2-thiouracil in drinking water), untreated control (EUT); hyperthyroid rats (HyperT, 0.25 mg/kg/day T4 s.c.) and vehicle-treated control rats. The latency of tumor appearance and the incidence and progression of tumors were determined. At sacrifice, blood samples were collected for hormone determinations and samples of tumor and mammary glands were obtained for immunohistological studies. HypoT rats had retarded growth and an increase in mammary fat. The latency was longer (p<0.0001), the incidence rate was lower (p<0.05) and tumor growth was slower in HypoT rats compared to EUT and HyperT rats. Mitotic index and PCNA immunostaining were similar in all groups. HypoT rats showed increased apoptosis (p<0.05) as evaluated by the apoptotic index and TUNEL staining. No differences in serum prolactin and progesterone were observed. However, circulating estradiol (E2) was significantly lower in HypoT and HyperT rats. Serum leptin levels were reduced in HypoT rats even though the abdominal fat mass was similar in all groups. To note, the leptin level was higher in HypoT rats that developed mammary tumors than the level in non-tumoral HypoT rats. In conclusion, hypothyroidism altered animal growth, breast morphology, body composition, leptin secretion and serum E2 enhancing apoptosis and, consequently, retarding mammary carcinogenesis in rats.

Relación entre el índice de masa corporal y antígeno prostático específico en varones libres de enfermedad prostática / Relationship between body mass index and prostate-specific antigen in men without prostatic diseases / Relação entre índice de massa corporal e antígeno prostático específico em homens livres de doença prostática

Introducción: Estudios recientes indican que los varones obesos tienen menor concentración plasmática de antígeno prostático específico (PSA) que los que tienen peso normal, posiblemente debido a un mayor volumen plasmático (hemodilución) y/o a una menor actividad androgénica, dificultando la detección precoz del câncer de próstata. No está establecido claramente si esta relación se acompaña de menores cantidades absolutas dePSA. El objetivo del presente trabajo fue determinar la asociación entre el índice de masa corporal (IMC), la concentración de PSA y sus cantidades absolutas circulantes (“PSA masa”). Material y Métodos: Se determinó PSA total en 570 varones de 45 a 80 años, con PSA considerado no sospecho-so de patologías prostáticas (<4ng/mL). Se evaluaron el peso, la talla y el IMC, se estimó el volumen plasmático (VP) y el PSA masa fue calculado a partir de la concentración plasmática de PSA y el VP. El análisis estadístico se realizó mediante coeficiente de correlación de Pearson o Spearman según la normalidad de las variables (p<0,05). Resultados: El IMC se asoció significativamente con un mayor VP (r = 0,512; p<0,0001). Dado que las concentraciones de PSA se asociaron positivamente con la edad (r = 0,248; p<0,0001), se analizaro...

Recent studies indicate that obese men have lower plasma prostate-specific antigen (PSA) concentrations than normal weight men, which may probably be explained by higher plasma volume (hemodilution) and/or a lower androgenic activity. This may interfere with the ability to detect early-stage prostate cancer. It is not clear whether this relationship is accompanied by lower absolute amounts of PSA. The aim of this study was to determine the association between the body mass index (BMI), the PSA concentrations and the totalamount of PSA in circulation (“PSA mass”). Material and methods: The total amount of PSA was determined in 570 men aged 45-80 years, whose PSA values were not indicators of prostate disease (<4ng/mL). Weight, height and BMI were measured, plasma volume(PV) was estimated, and PSA mass was calculated taking into account plasma PSA concentrations and PV. The statistical analysis was performed using Pearson orSpearman/'s correlation coefficient according to the normality of the variables (P<0.05). Results: The BMI was significantly associated with a higher PV (r = 0.512; P<0.0001). Due to the positive correlation between PSA concentrations and age (r = 0.248;P<0.0001), partial correlations adjusted for...

Estudos recentes indicam que os homens obesos têm menor concentração plasmática de antígeno prostático específico (PSA) que os que têm peso normal, possivelmente devido a um maior volume plasmático (hemodiluição) e/ou a uma menor atividade androgênica,dificultando a detecção precoce do câncer de próstata. Não está estabelecido claramente se esta relação está acompanhada de menores quantidades absolutas de PSA. O objetivo do presente trabalho foi determinar a associação entre o índice de massa corporal (IMC), a concentração de PSA e suas quantidades absolutas circulantes (/"PSA masa/"). Material e Métodos: Determinou-se PSA total em 570 homens de 45 a 80 anos, com PSA considerado não suspeitoso de patalogias prostáticas (<4ng/mL). Foram avaliados o peso, a altura e o IMC, estimou-se o volume plasmático (VP) e o PSA massa foi calculado a partir da concentração plasmática de PSA e o VP. A análise estatística foi realizada mediante coeficiente de correlação de Pearson ou Spearman segundo a normalidade das variáveis(p<0,05). Resultados: O IMC se associou significativamente com um maior VP (r = 0,512; p<0,0001). Dado que as concentrações de PSA se associaram positivamente com a idade (r = 0,248; p<0,0001), analisaram-se as correlações parciais corrigidas para esta variável. Assim, o IMC se associou com uma menor concentração de PSA (r = -0,298;p<0,0001) e menor PSA massa...

The inhibitory effect of progesterone on lactogenesis during pregnancy is already evident by mid- to late gestation in rodents.

Lactogenesis is a very complex process highly dependent on hormonal regulation. In the present study the time-course of the inhibitory actions of progesterone on prolactin secretion, mammary gland morphology and lactogenesis from mid- to late gestation in rodents was investigated. Groups of pregnant rats were luteectomised or administered with mifepristone on Day 10, 13, 15 or 17 of gestation and decapitated 28 or 48h later. Whole-blood samples and the inguinal mammary glands were taken for determinations of hormone levels and for measurement of mammary content of casein and lactose and for tissue morphology analyses, respectively. Luteectomy or mifepristone evoked prolactin increases only after Day 17 of gestation. Mammary content of casein was increased by both treatments regardless of timing or duration. Mifepristone was less effective than luteectomy in inducing lactose production and the effect was only observed after Day 15 of gestation. Analysis of mammary gland morphology confirmed the observed effect of progesterone on lactogenesis. Both treatments triggered remarkable secretory activity in the mammary gland, even without a parallel epithelial proliferation, demonstrating that the mammary epithelium is able to synthesise milk compounds long before its full lobulo-alveolar development is achieved, provided that progesterone action is abolished. Thus, the present study demonstrates that progesterone is a potent hormonal switch for the prolactin and prolactin-like effects on mammary gland development and its milk-synthesising capacity during pregnancy, and that its inhibitory action is already evident by mid-pregnancy in rodents.

El consumo elevado de licopeno sumado a una ingestión reducida de carnes rojas aumenta el poder antioxidante total

Los sistemas antioxidantes del cuerpo humano son capaces de remover a los radicales libres, protegiendo así al organismo del daño que estos pueden ocasionar, y pueden ser valorados en conjunto mediante la determinación del poder antioxidante total (TAS, por sus siglas en inglés). Este biomarcador es modulado por la alimentación mediante la incorporación de sustancias con propiedades antioxidantes o prooxidantes. El objetivo del presente trabajo fue estimar la ingestión de nutrientes antioxidantes y grupos específicos de alimentos y correlacionarla con el TAS. Fueron seleccionados al azar 45 sujetos de sexo masculino, entre 50 y 75 años, de una consulta médica de rutina. El trabajo consistió en una evaluación de TAS mediante técnica ABTS más una entrevista nutricional donde se evaluó la composición corporal mediante antropometría y la ingestión habitual de nutrientes y grupos específicos de alimentos mediante un recordatorio de 24 h y un cuestionario de frecuencia de consumo de alimentos validado para tal fin. El análisis estadístico se realizó mediante Coeficiente de Correlación de Pearson o Spearman según la normalidad de la muestra (p<0,05). El TAS se correlacionó positivamente con el consumo de licopeno (r=0,295; p=0,049) y negativamente con la ingestión de carnes rojas (r= -0,403; p=0,007). Los demás nutrientes o alimentos no se correlacionaron con el TAS. Por lo tanto, una ingestión elevada de licopeno y un consumo reducido de carnes rojas ayudarían a mejorar el sistema antioxidante del organismo.

High intake of lycopene together with low intake of red meat increases the total antioxidant status. The body's antioxidant systems are able to remove free radicals, thus protecting the body from the damage they may cause. They can be estimated, as a whole, through the determination of total antioxidant status (TAS). This biomarker can be modulated by dietary factors through the incorporation of substances with antioxidant or prooxidant properties. The aim of this study was to estimate the intake of antioxidant nutrients and specific food groups, and its correlation with TAS. Fortyfive male volunteers between 50 and 75 years were randomly selected from a medical consultation. The study included a TAS determination by ABTS and a nutritional interview where corporal composition was studied through anthropometry and the habitual consumption of nutrients was estimated by means of 24 hour diary and food consumption frequency questionnaire. Statistical analysis was performed by using Pearson or Spearman correlation coefficient (p <0.05). TAS was positively correlated with lycopene consumption (r=0,295; p=0,049), and negatively with red meat intake (r= -0,403; p= 0,007), while intake of other studied antioxidant nutrients did not correlate significantly with TAS. In conclusion, high intake of lycopene and reduced red meat consumption increase TAS.

[High intake of lycopene together with low intake of red meat increases the total antioxidant status]. / El consumo elevado de licopeno sumado a una ingestión reducida de carnes rojas aumenta el poder antioxidante total.

The body's antioxidant systems are able to remove free radicals, thus protecting the body from the damage they may cause. They can be estimated, as a whole, through the determination of total antioxidant status (TAS). This biomarker can be modulated by dietary factors through the incorporation of substances with antioxidant or prooxidant properties. The aim of this study was to estimate the intake of antioxidant nutrients and specific food groups, and its correlation with TAS. Forty-five male volunteers between 50 and 75 years were randomly selected from a medical consultation. The study included a TAS determination by ABTS and a nutritional interview where corporal composition was studied through anthropometry and the habitual consumption of nutrients was estimated by means of 24 hour diary and food consumption frequency questionnaire. Statistical analysis was performed by using Pearson or Spearman correlation coefficient (p < 0.05). TAS was positively correlated with lycopene consumption (r = 0.295; p = 0.049), and negatively with red meat intake (r = -0.403; p = 0.007), while intake of other studied antioxidant nutrients did not correlate significantly with TAS. In conclusion, high intake of lycopene and reduced red meat consumption increase TAS.

Regulation of prolactin secretion during the estrus in rats: possible role of glucocorticoids.

Mifepristone (MIF) administration to cycling rats at proestrus induces hypersecretion of prolactin (PRL) at the following estrus. We aimed to assess whether this effect is due to the antiprogesterone or antiglucocorticoid action of MIF and to help underscore the nature of the circulating hormone(s) regulating PRL secretion at estrus. Female cycling rats in proestrus were treated with vehicle; the progesterone (Pg) and glucocorticoid receptor antagonists, MIF (5 mg/kg) or ORG-33628 (5 mg/kg); the glucocorticoid agonist dexamethasone (DEX; 27 mg/kg)±MIF; or the inhibitor of steroid synthesis aminoglutethimide (AG; 150 mg/kg)±MIF. The animals' blood was sampled the same day at 1800 h and at 1800 h of the following day to assess for circulating PRL and Pg levels. To distinguish antiglucocorticoid from antiprogesterone effects of MIF, we administered a highly specific neutralizing antibody against Pg. None of the antagonists modified serum PRL values at proestrus but increased PRL levels at estrus. DEX decreased the secretion of PRL at proestrus, yet the effect was entirely blocked by MIF. Furthermore, DEX decreased PRL at estrus in a MIF-reversible manner, suggesting that adrenal corticoids during proestrous may regulate PRL secretion at estrus. AG increased PRL secretion at estrus, whereas its association with MIF produced an even higher response. PRL concentration at estrus was not modified by the antiprogesterone antibody, suggesting that the effect of MIF is a consequence of its antiglucocorticoid effect and not due to its antiprogesterone properties. In conclusion, PRL secretion in the afternoon of the estrus is most likely regulated by glucocorticoids through an inhibitory action.

Leptin increases prostate cancer aggressiveness.

Recent studies indicate that adipose tissue and adipocytokines might affect the development of prostate cancer (PCa). Leptin would have a stimulating effect on prostate cancer cells by inducing promotion and progression, whereas adiponectin would have a protective effect. The aim of this study was to determine the relation between body composition, leptin, and adiponectin levels with the prevalence and aggressiveness of PCa in men of Mendoza, Argentina. Seventy volunteers between 50 and 80 years (35 healthy men as control group and 35 with PCa) were selected. The PCa group was subclassified according to the Gleason Score (GS). Digital rectal examination, transrectal ultrasound, and prostatic biopsy were performed; PSA, testosterone, leptin, and adiponectin levels were determined; and a nutritional interview including anthropometric measurements and a food frequency questionnaire was carried out. Statistical analysis was performed by Student t test, ANOVA I, and Bonferroni (p < 0.05). Body mass index and percentage of body fat mass were not statistically different between PCa and control groups. However, body fat mass was higher in subjects with more aggressive tumors (p = 0.032). No differences were observed regarding leptin levels between the groups. Nevertheless, leptin levels were higher in subjects with high GS (p < 0.001). Adiponectin levels showed no statistical differences regarding the presence and aggressiveness of the tumor (p = 0.131). Finally, consumption and nutrient intake did not differ in the studied groups. In conclusion, body composition and leptin are related to the PCa aggressiveness but not with its prevalence.

Obesity modifies prostatic specific antigen in men over 45 years.

OBJECTIVES: To determine whether lower serum prostate-specific antigen (PSA) concentration in obese men is caused by plasma hemodilution and/or decreased serum testosterone levels. METHODS: A sample of 413 men, from 45 to 75 years old, were randomly selected for the study among those who participated in prostate cancer screening at 2 urban urology practices in Argentina and Puerto Rico. Weight, height, serum testosterone and total PSA concentration were determined. Body mass index (BMI), body surface, plasma volume, and PSA mass were calculated. Prostate volume was estimated by transrectal ultrasound using the prolate ellipsoid formula. RESULTS: Mean age was 59 years old (range, 45 to 75) and mean BMI was 28.8 kg/m2 (range, 24 to 46). Mean serum PSA concentration was 1.43 ng/ml in normal weight patients (n=68), 1.4 ng/ml in overweight patients (n=222), 1.05 ng/ml in obese patients (n=114), and 0.85 ng/ml in morbidly obese patients (n=9). BMI was directly correlated with plasma volume (r= 0.687; p= 0.001) and inversely correlated with serum PSA concentration (r= -0.235; P= 0.001). PSA mass tended to be lower in obese and morbidly obese patients (P= 0.0063)compared to normal weight and overweight subjects. Serum testosterone concentration (P= 0.91) and prostate volume (P= 0.068) were similar among all BMI groups. CONCLUSIONS: Obese men had lower serum PSA concentrations than normal weight men mainly due to plasma hemodilution. PSA mass tended to be lower in obese patients, but it is unlikely a consequence of lower serum testosterone concentrations.

[Body mass index and diet affect prostate cancer development]. / El indice de masa corporal y la dieta afectan el desarrollo del cancer de próstata.

INTRODUCTION: Prostate cancer (CaP) is one of the most important causes of morbidity and mortality in the world. There is evidence that obesity and inadequate eating habits may promote CaP development. OBJECTIVE: To analyze and compare the body mass index (BMI) and the food intake, especially fats and antioxidants, among subjects with CaP and those free of disease as a control group. MATERIAL AND METHODS: A sample of 40 men between 50 and 80 years old were selected for the study: 20 with CaP and 20 healthy men as control group. All volunteers underwent a digital rectal examination, prostate specific antigen level, ultrasound and transrectal prostate biopsy, and a nutritional interview where a dietary history and different anthropometric measurements were made. Statistical analysis was performed using the Student T test for independent samples (p < 0.05). RESULTS: BMI in the subjects with CaP was higher than in controls (29.8 kg/m2 vs. 27.96 kg/m2, p = 0.13) but not statistically significant. However, there was a direct correlation between BMI and tumor aggressiveness (r = 0.79, P < 0.001). Total, saturated, monounsaturated and polyunsaturated fat intake was significantly higher in subjects with CaP; while omega3 fatty acids, vitamin C and lycopene intake was significantly lower than in controls (p < 0.05). CONCLUSIONS: A healthy weight and a diet low in total fat, saturated, monounsaturated and polyunsaturated fat and rich in n3 fatty acids, vitamin C and lycopene is associated with a lower risk of CaP.

[Advances on the influence of adipose tissue on prostate cancer]. / Avances sobre la influencia del tejido adiposo en el adenocarcinoma de próstata.

UNLABELLED: Numerous studies have investigated the association between obesity and prostate cancer (CaP), although the results have not been concluding due to the great difficulty to evaluate the effects of obesity on the development of this type of tumor. The aim of this study was to carry out a comprehensive over-view of the existing evidence about the role of adipose tissue in the prostate carcinogenesis. Recent evidence suggests that androgens, leptin, IL-6, VEGF, insulin and IGF-1 may play a role in PC progression, while adiponectin and IGFBP-3 may act as "anti-prostatic cancer" adipokines. The potential mechanisms by which obesity may initiate, promote or facilitate the progression of CaP are low levels of testosterone and high levels of estrogen, coexisting metabolic syndrome, increased secretion of leptin, VEGF, IL-6 and TNF-alpha and decreased adiponectin, and excessive intake of saturated fat. CONCLUSION: Obesity may promote the progression of established PC rather than being a risk factor for the development of this tumour. However, additional studies are needed to clarify the relationship between adipokines and PC before developing new preventive or treatment strategies for this tumor.

[Influence of leptin and adiponectin on prostate cancer]. / Influencia de la leptina y adiponectina en el cáncer de próstata.

BACKGROUND: Many studies have investigated the association between obesity, adipose tissue-derived factors (leptin and adiponectin) and prostate cancer (CaP) but the results are still inconsistent. METHODS: The aim of this study was to carry out a comprehensive review of the existing evidence about the role of leptin and adiponectin in prostate carcinogenesis and to provide an overview of it. RESULTS: Recent evidence suggests that leptin may play a rol in prostate cancer progression, while adiponectin may act as an "antiprostatic cancer" adipokine. CONCLUSIONS: Obesity may promote the progression of established prostate cancer and and adipokines may provide a molecular mechanism whereby obesity exerts its effects on prostate tumour biology.