Ignet

Gene Information

Gene symbol: CSH1

Gene name: chorionic somatomammotropin hormone 1 (placental lactogen)

HGNC ID: 2440

Synonyms: hCS-A, CSA, PL, CSMT, FLJ75407

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	AFP	1 hits
3	ALPP	1 hits
4	APOE	1 hits
5	BEST1	1 hits
6	BRD2	1 hits
7	CDKN1A	1 hits
8	CFD	1 hits
9	CGB	1 hits
10	CGB5	1 hits
11	CSH2	1 hits
12	GH1	1 hits
13	GH2	1 hits
14	GHR	1 hits
15	HGF	1 hits
16	IDDM2	1 hits
17	IGF1	1 hits
18	IGF2	1 hits
19	INS	1 hits
20	LEP	1 hits
21	PAPPA	1 hits
22	POMC	1 hits
23	PRL	1 hits
24	PSG1	1 hits
25	PSG5	1 hits
26	PTH	1 hits
27	PTHLH	1 hits
28	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	63107	Prediction of fetal outcome by urinary estriol, maternal serum placental lactogen, and alpha-fetoprotein in diabetes and hepatosis of pregnancy.
2	63107	Urinary estriol, serum placental lactogen (hPL), and alphafetoprotein (AFP) levels were investigated in singleton pregnancies of 75 diabetic women and 84 women with obstetric hepatosis.
3	63107	Prediction of fetal outcome by urinary estriol, maternal serum placental lactogen, and alpha-fetoprotein in diabetes and hepatosis of pregnancy.
4	63107	Urinary estriol, serum placental lactogen (hPL), and alphafetoprotein (AFP) levels were investigated in singleton pregnancies of 75 diabetic women and 84 women with obstetric hepatosis.
5	707588	Insulin requirements were unrelated to plasma growth hormone, placental lactogen, or glucagon concentrations.
6	879249	In twin pregnancies, the PAPP-A, PAPP-C, and human placental lactogen levels were all increased, particularly PAPP-A.
7	1032812	Plasma glucose, plasma immunoreactive insulin and plasma placental lactogen (HPL) levels were measured before (fasting) and at timed intervals after the glucose challenge; the glucose response was expressed as the increment index.
8	1280539	Amniotic fluid (AF) and maternal serum (MS) chorionic gonadotropin (HCG), placental lactogen (HPL), pregnancy-specific beta 1-glycoprotein (SP1), total estrogens (ET), alpha-fetoprotein (AFP) and prolactin (PRL) were measured by enzyme-immunoassays, in 50 normal (A) and in 37 abnormal (B) pregnancies, from 16th to 40th weeks.
9	1280539	A: the proteins HCG, AFP and PRL showed a similar decreasing trend after the 20th week, while HPL and SP1 rose progressively throughout the 2nd trimester, thereafter remaining constant.
10	1280539	Chorionic gonadotropin HPL and SP1 in MS were higher than in AF, while AF values of AFP and PRL were higher than in MS, but the ratio MS/AF of all hormone values increased significantly from the 2nd to the 3rd trimester (p < 0.005-p < 0.000001).
11	1280539	In erythroblastosis and diabetes, AFP was very low, but placental hormones, PRL and ET were both high and low.
12	1280539	In toxemia, SP1, hCG and PRL were elevated, while HPL and ET were very low.
13	1294434	Pregnancy is a state of natural insulin resistance, which is due to placental production of human placental lactogen (HPL), an insulin antagonising hormone, leading to a remarkable increase of insulin requirement in pregnant diabetics in the 2nd and 3rd trimester.
14	2091054	The ability of insulin-dependent diabetic (IDDM) women to breast-feed has been documented, however, there is little information concerning milk composition or factors that influence successful breastfeeding.
15	2091054	Placental lactogen and prolactin levels can be normalized during pregnancy with good metabolic control.
16	2091054	Prolactin maintains mammary gland insulin receptors to ensure anabolism.
17	2091054	Lactation in IDDM women may be influenced by hyper- or hypoglycemia as women balance their insulin needs.
18	2481301	We correlated the villous histology with the immunocytochemical distribution of four trophoblastic proteins: beta human chorionic gonadotropin (beta HCG), placental alkaline phosphatase (PLAP), pregnancy specific beta-1-glycoprotein (SP1), and human placental lactogen (HPL) in 14 third-trimester placentas associated with diabetes mellitus.
19	2481301	Staining was increased for beta HCG and decreased for PLAP, SP1, and HPL in the diabetic placentas compared to control placentas of similar gestational age.
20	2670532	[Growth hormone, insulin and placental lactogen in the sera of mothers and fetal blood of infants from physiological pregnancy and pregnancy complicated by diabetes mellitus].
21	2670532	The study was aimed at investigating the changes in the blood serum concentrations of growth hormone (HGH), insulin and placental lactogen (HPL) in the newborns of diabetic mothers as compared to those born from physiological pregnancies.
22	2670532	[Growth hormone, insulin and placental lactogen in the sera of mothers and fetal blood of infants from physiological pregnancy and pregnancy complicated by diabetes mellitus].
23	2670532	The study was aimed at investigating the changes in the blood serum concentrations of growth hormone (HGH), insulin and placental lactogen (HPL) in the newborns of diabetic mothers as compared to those born from physiological pregnancies.
24	2751954	Serum progesterone, oestradiol, human chorionic gonadotrophin (hCG) and human placental lactogen (hPL) were determined serially throughout 27 pregnancies in insulin-dependent diabetic patients from Newcastle (UK), 15 such patients from Stockholm (Sweden) and in 69 normal women having uncomplicated pregnancies.
25	2783318	Serum concentrations of hCG, pregnancy-specific beta-1-glycoprotein, placental lactogen, and hCG alpha were measured serially.
26	3290008	These animals have high plasma lactogen levels in the form of placental lactogen, increased plasma insulin, and decreased plasma glucose.
27	3515818	Previous studies have shown that progesterone and human placental lactogen (hPL) had direct effects on isolated islets and in the present study the effects of combined addition of these hormones to the cultured islets were evaluated. hPL, 1 microgram/ml was found to prevent the decrease in the islet insulin content due to progesterone 100 ng/ml, and hPL induced an increase in the DNA-content compared with the progesterone treated islets.
28	3519044	The possible involvement of growth hormone (GH) and human placental lactogen (HPL) in the development of diabetic tissue damage during pregnancy was studied in 16 insulin-dependent diabetic patients (IDDM), 8 gestational diabetic patients (GD) and 14 normal pregnant women.
29	3519044	HPL was positively correlated with urinary albumin excretion (UAE) in all 3 groups, but with blood pressure only in the IDDM group.
30	3908179	The increased insulin responsiveness seems to be caused by pregnancy-related changes in the secretion of progesterone, estradiol, human placental lactogen (hPL) and prolactin.
31	3922827	Results show that the birth weight and/or birth weight ratio are weakly positively associated with maternal very-low-density lipoprotein (VLDL) triglyceride and statistically significantly positively associated with apoprotein A-I, placental lactogen, estradiol, bilirubin, and maternal prepregnancy weight and pregnancy weight gain.
32	3922827	Significant negative predictors of birth weight or birth weight ratio include VLDL cholesterol, apoprotein A-II, SGOT, and creatinine.
33	3972153	Human placental lactogen (hPL), a hormone similar to growth hormone, is produced by the placenta and is a potent antagonist to insulin action.
34	4050920	Nonsuppressible insulin-like activity and somatomedin C levels in normal pregnant women, in pregnant women with gestational diabetes, and in umbilical cord blood of mature and premature infants.
35	4050920	This study was undertaken to determine the significance of the changes in nonsuppressible insulin-like activity as measured by the fat pad assay and by the levels of immunoreactive somatomedin C, growth hormone, and human placental lactogen in sera of term normal pregnant women, mothers who delivered prematurely, and women with gestational diabetes at term as compared to normal nonpregnant subjects.
36	4050920	Our investigations showed that (1) nonsuppressible insulin-like activity is elevated during pregnancy, but its level was lower in mothers with gestational diabetes in spite of significantly higher serum human placental lactogen compared with normal pregnant mothers; (2) nonsuppressible insulin-like activity is significantly lower in premature infants than in term infants; (3) somatomedin C levels were significantly elevated in pregnant mothers in spite of suppression of growth hormone; (4) nonsuppressible insulin-like activity and somatomedin C levels in infants of mothers with gestational diabetes were not significantly elevated in spite of higher birth weight, indicating that nonsuppressible insulin-like activity and somatomedins are not the only factors responsible for the increase of birth weight of children of diabetic mothers; (5) there was marked discordance between the growth hormone level in the neonates and somatomedin C levels.
37	4050920	Nonsuppressible insulin-like activity and somatomedin C levels in normal pregnant women, in pregnant women with gestational diabetes, and in umbilical cord blood of mature and premature infants.
38	4050920	This study was undertaken to determine the significance of the changes in nonsuppressible insulin-like activity as measured by the fat pad assay and by the levels of immunoreactive somatomedin C, growth hormone, and human placental lactogen in sera of term normal pregnant women, mothers who delivered prematurely, and women with gestational diabetes at term as compared to normal nonpregnant subjects.
39	4050920	Our investigations showed that (1) nonsuppressible insulin-like activity is elevated during pregnancy, but its level was lower in mothers with gestational diabetes in spite of significantly higher serum human placental lactogen compared with normal pregnant mothers; (2) nonsuppressible insulin-like activity is significantly lower in premature infants than in term infants; (3) somatomedin C levels were significantly elevated in pregnant mothers in spite of suppression of growth hormone; (4) nonsuppressible insulin-like activity and somatomedin C levels in infants of mothers with gestational diabetes were not significantly elevated in spite of higher birth weight, indicating that nonsuppressible insulin-like activity and somatomedins are not the only factors responsible for the increase of birth weight of children of diabetic mothers; (5) there was marked discordance between the growth hormone level in the neonates and somatomedin C levels.
40	4700328	Those patients requiring the largest insulin increment for the control of their diabetes in the pregnancy have placental lactogen levels in the higher range.
41	4724402	Human placental lactogen levels and daily insulin requirements in patients with diabetes mellitus complicating pregnancy.
42	5110702	Patterns of serum immunoreactive human placental lactogen (IR-HPL) and chorionic gonadotropin (IR-HCG) in diabetic pregnancy.
43	6096045	Both insulin and the related peptides, the insulin-like growth factors/somatomedins, may function as anabolic factors in the regulation of fetal body size.
44	6096045	Insulin-like growth factors I (IGFI) and II are present in the circulation of the newborn infant and animal fetus and correlate positively with birth size.
45	6096045	The fetal tissues are biologically responsive to IGFs in vitro and are rich in specific cell membrane receptors, those predominantly recognizing IGFI being structurally and functionally similar to the insulin receptor.
46	6096045	Fetal IGF production may be influenced by placental lactogen, especially IGFII which rapidly declines in the circulation following parturition in the rat and sheep.
47	6096045	Similarly the infant born with transient diabetes mellitus has low cord blood levels of insulin and IGFI.
48	6135831	Serum human placental lactogen (hPL) and human chorionic gonadotropin (hCG) were assayed and fetal crown-rump length (CRL) was determined by sonar in three groups of pregnant women--35 with uncomplicated pregnancies, 13 with insulin-dependent diabetes mellitus, and 21 who represented a general pregnancy population.
49	6378262	Levels of human placental lactogen (HPL) were significantly elevated in B-noRx patients compared to PC and A and were lowered to levels comparable to normal in insulin-treated B patients.
50	6378262	Elevations of pregnancy-specific beta 1 glycoprotein were observed in patients with mild carbohydrate intolerance (A) as well as Bno-Rx, but were comparable to normal in those B-patients receiving insulin therapy.
51	6457170	The comparative study between 6059-S, SBPC and ABPC was performed by various hormone level, including E3 (blood and urine), blood progesterone, alpha-fetoprotein, human chorionic gonadotropin (HCG), cortisol and human placental lactogen (HPL). 9 cases of intrauterine fetal growth retardation (IUGR) (ranging from 28 approximately 36 weeks of pregnancy) was selected, including toxemia of pregnancy or complicated pregnancy of myoma of uterus and diabetes mellitus.
52	6734879	Placental lactogen, progesterone, total estriol and prolactin plasma levels in pregnant women with insulin-dependent diabetes mellitus.
53	6787188	Sp1, the pregnancy-specific beta 1-glycoprotein, was studied in normal and pathologic pregnancies.
54	6787188	Since the radioimmunological determination of SP1 is possible in the early stage of gestation (from week 8) it may serve as a useful tool for prediction at times when the determination of placental lactogen is not yet possible.
55	6787188	Serial determinations of SP1 in the serum of women with EPH-gestosis were compared with the corresponding HPL determinations and showed the equality of SP1 concerning the assessment of the placental function.
56	7095333	The occurrence and progression of retinopathy were related to the mean blood glucose levels and the serum concentrations of prolactin, human placental lactogen, oestradiol and progesterone in 57 pregnant insulin-dependent diabetic patients.
57	8001865	Growth hormone-binding protein in plasma is inversely correlated to placental lactogen and augmented with increasing body mass index in healthy pregnant women and women with gestational diabetes mellitus.
58	8001865	Pituitary growth hormone (GH), prolactin (PRL), placental lactogen (PL), insulin-like growth factor 1 (IGF-1) and GH-binding protein (GHBP) in plasma were determined in 12 women with gestational diabetes mellitus (GDM) and in 12 healthy pregnant women during a breakfast meal tolerance test.
59	8001865	No difference was found between the two groups in pituitary GH, PRL, PL and IGF-1 levels.
60	8001865	Growth hormone-binding protein in plasma is inversely correlated to placental lactogen and augmented with increasing body mass index in healthy pregnant women and women with gestational diabetes mellitus.
61	8001865	Pituitary growth hormone (GH), prolactin (PRL), placental lactogen (PL), insulin-like growth factor 1 (IGF-1) and GH-binding protein (GHBP) in plasma were determined in 12 women with gestational diabetes mellitus (GDM) and in 12 healthy pregnant women during a breakfast meal tolerance test.
62	8001865	No difference was found between the two groups in pituitary GH, PRL, PL and IGF-1 levels.
63	8115596	Placental hormones, including human chorionic gonadotropin (hCG) and human placental lactogen (hPL), are predicted to manipulate maternal physiology for fetal benefit.
64	8238332	Throughout gestation, maternal insulin-like growth factor I (IGF-I) increases progressively despite suppressed pituitary growth hormone (GH) secretion.
65	8238332	We have previously shown that in normal pregnancy, a specific placental GH variant, rather than human placental lactogen (hPL), substitutes for pituitary GH in the regulation of maternal IGF-I.
66	8372111	Adipsin expression and growth in rats as influenced by insulin and somatotropin.
67	8372111	Insulin reduces adipsin expression in vitro and is negatively correlated with adipsin expression in vivo.
68	8372111	Because bovine somatotropin (bST) opposes many actions of insulin and can reduce body fat content, we tested the hypothesis that bST enhances adipsin expression.
69	8372111	In two experiments using 210 rats, bST and a similar hormone, bovine placental lactogen (bPL), both caused a small (14 to 27%) but statistically significant reduction in circulating adipsin protein.
70	8477657	In the presence of 10 micrograms/liter insulin, 50 micrograms/liter insulin-like growth factor-1 did not alter the ability of GH to suppress lipid accumulation.
71	8477657	Human placental lactogen and hLH, hFSH, and hTSH did not cross-react with GH in this assay.
72	8942023	Pregnancy itself is diabetogenic caused by increased insulin resistance due to the production of hormones like estrogen, progesterone, cortisol, human chorionic somatomammotropin (hCS) and human placental lactogen (hPL).
73	9704223	Similar frequencies of HLA-DR2, DR3, and DR4 antigens in healthy pregnant women and women with GDM and low prevalences of markers for autoimmune destruction of the beta-cells in GDM pregnancy rule out the possibility that GDM is a disease of autoimmune origin.
74	9704223	Insulin receptor binding to target tissues is largely unaffected by normal and GDM pregnancy; the same is true for basal and insulin-stimulated insulin receptor-bound tyrosine kinase activity.
75	9704223	Hormones that circulate in high concentrations in pregnancy (e.g., progesterone, cortisol, prolactin, human placental lactogen, and estrogen) have all been shown, in animal models, to be able to influence beta-cell function and/or the peripheral tissue sensitivity to insulin, but whether they play similar roles in human pregnancy remains to be investigated.
76	9930929	Increased mitotic activity has been seen both in vivo and in vitro in islets exposed to placental lactogen (PL), prolactin (PRL) and growth hormone (GH).
77	9930929	Thus the mitotic signaling only requires the membrane proximal part of the receptor and activation of the tyrosine kinase JAK2 and the transcription factors STAT1 and 3.
78	9930929	In order to identify putative autocrine growth factors or targets for growth factors we have cloned a novel GH/PRL stimulated rat islet gene product, Pref-1 (preadipocyte factor-1).
79	10619404	The human growth hormone/chorionic somatomammotropin (hGH/CS) family consists of five genes, one of which (GH-N) is expressed efficiently in pituitary while the other four (CS-A, B, L, and hGH-V) are expressed in placenta and represent ultimate placental differentiation markers.
80	10619404	Specifically, normal term placentas express higher relative levels of hCS-L, lower relative hGH-V levels and a 70-fold lower hGH-V/CS-L mRNA ratio compared to early placentas.
81	10619404	Also, many term placentas from diabetic pregnancies express lower relative levels of hCS-L mRNA and a much higher hGH-V/CS-L mRNA ratio compared to normal term placenta, resembling more an early placenta pattern of expression.
82	10671817	Basal levels of adrenocorticotropic hormone, cortisol, growth hormone, insulin-like growth factor-I, prolactin, glucagon, estradiol, progesterone, human placental lactogen and human chorionic gonadotropin were investigated in 15 nonobese women with GDM and 26 matched normal pregnant women (N).
83	10809775	In order to explore the role of murine placental lactogen (PL)-I (mPL-I) in islet mass regulation in vivo, we developed transgenic mice in which mPL-I is targeted to the beta cell using the rat insulin II promoter.
84	11723058	We have developed three transgenic models in which growth factors (hepatocyte growth factor [HGF], placental lactogen, or parathyroid hormone-related protein) have been targeted to the beta-cell using rat insulin promoter (RIP).
85	11723058	RIP-HGF islets, P < 0.01), have two- to threefold higher GLUT2 and glucokinase steady-state mRNA levels, take up and metabolize glucose more effectively, and most importantly, function at least twice as effectively after transplantation.
86	12086951	TNF-alpha is a predictor of insulin resistance in human pregnancy.
87	12086951	The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha.
88	12086951	Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps.
89	12086951	TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001).
90	12086951	During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006).
91	12086951	Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02).
92	12086951	Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01).
93	12086951	These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy.
94	15561942	Characterization of mice doubly transgenic for parathyroid hormone-related protein and murine placental lactogen: a novel role for placental lactogen in pancreatic beta-cell survival.
95	15561942	Transgenic overexpression of either parathyroid hormone-related peptide (PTHrP) or mouse placental lactogen type 1 (mPL1) in pancreatic beta-cells, using the rat insulin II promoter (RIP), results in islet hyperplasia either through prolonged beta-cell survival or through increased beta-cell proliferation and hypertrophy, respectively.
96	15561942	Characterization of mice doubly transgenic for parathyroid hormone-related protein and murine placental lactogen: a novel role for placental lactogen in pancreatic beta-cell survival.
97	15561942	Transgenic overexpression of either parathyroid hormone-related peptide (PTHrP) or mouse placental lactogen type 1 (mPL1) in pancreatic beta-cells, using the rat insulin II promoter (RIP), results in islet hyperplasia either through prolonged beta-cell survival or through increased beta-cell proliferation and hypertrophy, respectively.
98	16380478	Evaluation of beta-cell replication in mice transgenic for hepatocyte growth factor and placental lactogen: comprehensive characterization of the G1/S regulatory proteins reveals unique involvement of p21cip.
99	16380478	We hypothesized that combined transgenic overexpression of hepatocyte growth factor (HGF) and placental lactogen in islets would lead to even greater increases in beta-cell mass and replication than either growth factor alone.
100	16380478	We therefore performed the first comprehensive G(1)/S cell cycle survey in islets, cataloguing the broad range of kinases, cyclins, and kinase inhibitors that control the G(1)/S transition in islets from normal, HGF, placental lactogen, and doubly transgenic mice.
101	16380478	Many of the G(1)/S checkpoint regulators (E2Fs; pRb; p107; p130; cyclins D(1),(2),(3), A, and E; cdk-2; cdk-4; p15; p16; p18; p19; p21; p27; MDM2; p53; c-Myc; and Egr-1) are present in the murine islet.
102	16380478	Most of these proteins were unaltered by overexpression of HGF or placental lactogen, either alone or in combination.
103	16380478	In contrast, p21(cip) was uniquely, dramatically, and reproducibly upregulated in placental lactogen and HGF islets. p21(cip) was also present in, and upregulated in, proliferating human islets, localizing specifically in beta-cells and translocating to the nucleus on mitogenic stimulation.
104	16380478	Homozygous p21(cip) loss releases islets from growth inhibition, markedly enhancing proliferation in response to HGF and placental lactogen.
105	16380478	Evaluation of beta-cell replication in mice transgenic for hepatocyte growth factor and placental lactogen: comprehensive characterization of the G1/S regulatory proteins reveals unique involvement of p21cip.
106	16380478	We hypothesized that combined transgenic overexpression of hepatocyte growth factor (HGF) and placental lactogen in islets would lead to even greater increases in beta-cell mass and replication than either growth factor alone.
107	16380478	We therefore performed the first comprehensive G(1)/S cell cycle survey in islets, cataloguing the broad range of kinases, cyclins, and kinase inhibitors that control the G(1)/S transition in islets from normal, HGF, placental lactogen, and doubly transgenic mice.
108	16380478	Many of the G(1)/S checkpoint regulators (E2Fs; pRb; p107; p130; cyclins D(1),(2),(3), A, and E; cdk-2; cdk-4; p15; p16; p18; p19; p21; p27; MDM2; p53; c-Myc; and Egr-1) are present in the murine islet.
109	16380478	Most of these proteins were unaltered by overexpression of HGF or placental lactogen, either alone or in combination.
110	16380478	In contrast, p21(cip) was uniquely, dramatically, and reproducibly upregulated in placental lactogen and HGF islets. p21(cip) was also present in, and upregulated in, proliferating human islets, localizing specifically in beta-cells and translocating to the nucleus on mitogenic stimulation.
111	16380478	Homozygous p21(cip) loss releases islets from growth inhibition, markedly enhancing proliferation in response to HGF and placental lactogen.
112	16380478	Evaluation of beta-cell replication in mice transgenic for hepatocyte growth factor and placental lactogen: comprehensive characterization of the G1/S regulatory proteins reveals unique involvement of p21cip.
113	16380478	We hypothesized that combined transgenic overexpression of hepatocyte growth factor (HGF) and placental lactogen in islets would lead to even greater increases in beta-cell mass and replication than either growth factor alone.
114	16380478	We therefore performed the first comprehensive G(1)/S cell cycle survey in islets, cataloguing the broad range of kinases, cyclins, and kinase inhibitors that control the G(1)/S transition in islets from normal, HGF, placental lactogen, and doubly transgenic mice.
115	16380478	Many of the G(1)/S checkpoint regulators (E2Fs; pRb; p107; p130; cyclins D(1),(2),(3), A, and E; cdk-2; cdk-4; p15; p16; p18; p19; p21; p27; MDM2; p53; c-Myc; and Egr-1) are present in the murine islet.
116	16380478	Most of these proteins were unaltered by overexpression of HGF or placental lactogen, either alone or in combination.
117	16380478	In contrast, p21(cip) was uniquely, dramatically, and reproducibly upregulated in placental lactogen and HGF islets. p21(cip) was also present in, and upregulated in, proliferating human islets, localizing specifically in beta-cells and translocating to the nucleus on mitogenic stimulation.
118	16380478	Homozygous p21(cip) loss releases islets from growth inhibition, markedly enhancing proliferation in response to HGF and placental lactogen.
119	16380478	Evaluation of beta-cell replication in mice transgenic for hepatocyte growth factor and placental lactogen: comprehensive characterization of the G1/S regulatory proteins reveals unique involvement of p21cip.
120	16380478	We hypothesized that combined transgenic overexpression of hepatocyte growth factor (HGF) and placental lactogen in islets would lead to even greater increases in beta-cell mass and replication than either growth factor alone.
121	16380478	We therefore performed the first comprehensive G(1)/S cell cycle survey in islets, cataloguing the broad range of kinases, cyclins, and kinase inhibitors that control the G(1)/S transition in islets from normal, HGF, placental lactogen, and doubly transgenic mice.
122	16380478	Many of the G(1)/S checkpoint regulators (E2Fs; pRb; p107; p130; cyclins D(1),(2),(3), A, and E; cdk-2; cdk-4; p15; p16; p18; p19; p21; p27; MDM2; p53; c-Myc; and Egr-1) are present in the murine islet.
123	16380478	Most of these proteins were unaltered by overexpression of HGF or placental lactogen, either alone or in combination.
124	16380478	In contrast, p21(cip) was uniquely, dramatically, and reproducibly upregulated in placental lactogen and HGF islets. p21(cip) was also present in, and upregulated in, proliferating human islets, localizing specifically in beta-cells and translocating to the nucleus on mitogenic stimulation.
125	16380478	Homozygous p21(cip) loss releases islets from growth inhibition, markedly enhancing proliferation in response to HGF and placental lactogen.
126	16380478	Evaluation of beta-cell replication in mice transgenic for hepatocyte growth factor and placental lactogen: comprehensive characterization of the G1/S regulatory proteins reveals unique involvement of p21cip.
127	16380478	We hypothesized that combined transgenic overexpression of hepatocyte growth factor (HGF) and placental lactogen in islets would lead to even greater increases in beta-cell mass and replication than either growth factor alone.
128	16380478	We therefore performed the first comprehensive G(1)/S cell cycle survey in islets, cataloguing the broad range of kinases, cyclins, and kinase inhibitors that control the G(1)/S transition in islets from normal, HGF, placental lactogen, and doubly transgenic mice.
129	16380478	Many of the G(1)/S checkpoint regulators (E2Fs; pRb; p107; p130; cyclins D(1),(2),(3), A, and E; cdk-2; cdk-4; p15; p16; p18; p19; p21; p27; MDM2; p53; c-Myc; and Egr-1) are present in the murine islet.
130	16380478	Most of these proteins were unaltered by overexpression of HGF or placental lactogen, either alone or in combination.
131	16380478	In contrast, p21(cip) was uniquely, dramatically, and reproducibly upregulated in placental lactogen and HGF islets. p21(cip) was also present in, and upregulated in, proliferating human islets, localizing specifically in beta-cells and translocating to the nucleus on mitogenic stimulation.
132	16380478	Homozygous p21(cip) loss releases islets from growth inhibition, markedly enhancing proliferation in response to HGF and placental lactogen.
133	16380478	Evaluation of beta-cell replication in mice transgenic for hepatocyte growth factor and placental lactogen: comprehensive characterization of the G1/S regulatory proteins reveals unique involvement of p21cip.
134	16380478	We hypothesized that combined transgenic overexpression of hepatocyte growth factor (HGF) and placental lactogen in islets would lead to even greater increases in beta-cell mass and replication than either growth factor alone.
135	16380478	We therefore performed the first comprehensive G(1)/S cell cycle survey in islets, cataloguing the broad range of kinases, cyclins, and kinase inhibitors that control the G(1)/S transition in islets from normal, HGF, placental lactogen, and doubly transgenic mice.
136	16380478	Many of the G(1)/S checkpoint regulators (E2Fs; pRb; p107; p130; cyclins D(1),(2),(3), A, and E; cdk-2; cdk-4; p15; p16; p18; p19; p21; p27; MDM2; p53; c-Myc; and Egr-1) are present in the murine islet.
137	16380478	Most of these proteins were unaltered by overexpression of HGF or placental lactogen, either alone or in combination.
138	16380478	In contrast, p21(cip) was uniquely, dramatically, and reproducibly upregulated in placental lactogen and HGF islets. p21(cip) was also present in, and upregulated in, proliferating human islets, localizing specifically in beta-cells and translocating to the nucleus on mitogenic stimulation.
139	16380478	Homozygous p21(cip) loss releases islets from growth inhibition, markedly enhancing proliferation in response to HGF and placental lactogen.
140	17130470	We next attempted to drive beta-cell replication in p21-null mice by crossing them with rat insulin II promoter-murine PL-1 (islet-targeted placental lactogen transgenic) mice.
141	17130470	A G(1/S) proteome scan demonstrated that p21(cip1) loss was not associated with compensatory increases in other cell cycle inhibitors (pRb, p107, p130, p16, p19, and p27), although mild increases in p57 were apparent.
142	17130470	In summary, isolated p21(cip1) loss, as for pRb, p53, p18, and p27 and other inhibitors, results in normal beta-cell development and function, either because it is not essential or because its function is subserved or complimented by another protein.
143	17728251	Lactogens promote beta cell survival through JAK2/STAT5 activation and Bcl-XL upregulation.
144	17728251	This study explores the role of lactogenic hormones, prolactin (PRL) and placental lactogen (PL), in beta cell survival.
145	17728251	We have previously shown that transgenic mice expressing mouse placental lactogen-1 (mPL1) in beta cells under the rat insulin II promoter (RIP) are resistant to the diabetogenic and cytotoxic effects of streptozotocin (STZ) in vivo.
146	17728251	The signaling pathway mediating this protective effect is the janus-activated-kinase-2/signal transducer and activator of transcription-5 (JAK2/STAT5) pathway.
147	17728251	This is demonstrated in INS-1 cells and primary mouse beta cells using three separate approaches, pharmacological inhibitors, JAK2-specific siRNAs and a dominant-negative STAT5 mutant.
148	17728251	We believe this is the first direct demonstration of lactogens mediating their protective effect through the JAK2/STAT5 pathway in the beta cell and through Bcl-XL in any cell type.
149	17728251	Lactogens promote beta cell survival through JAK2/STAT5 activation and Bcl-XL upregulation.
150	17728251	This study explores the role of lactogenic hormones, prolactin (PRL) and placental lactogen (PL), in beta cell survival.
151	17728251	We have previously shown that transgenic mice expressing mouse placental lactogen-1 (mPL1) in beta cells under the rat insulin II promoter (RIP) are resistant to the diabetogenic and cytotoxic effects of streptozotocin (STZ) in vivo.
152	17728251	The signaling pathway mediating this protective effect is the janus-activated-kinase-2/signal transducer and activator of transcription-5 (JAK2/STAT5) pathway.
153	17728251	This is demonstrated in INS-1 cells and primary mouse beta cells using three separate approaches, pharmacological inhibitors, JAK2-specific siRNAs and a dominant-negative STAT5 mutant.
154	17728251	We believe this is the first direct demonstration of lactogens mediating their protective effect through the JAK2/STAT5 pathway in the beta cell and through Bcl-XL in any cell type.
155	19292617	Femur BMD, CSA, and SM were larger in women with higher BMI, but values scaled in proportion to lean and not to fat or total body mass.
156	19292617	BMD, CSA, and SM vary in proportion to total body lean mass, supporting the view that bones adapt to prevalent muscle loads.
157	19292617	Because lean mass is a progressively smaller fraction of total mass in obesity, femur BMD, CSA, and SM decline relative to body weight in higher BMI categories.
158	19292617	Femur BMD, CSA, and SM were larger in women with higher BMI, but values scaled in proportion to lean and not to fat or total body mass.
159	19292617	BMD, CSA, and SM vary in proportion to total body lean mass, supporting the view that bones adapt to prevalent muscle loads.
160	19292617	Because lean mass is a progressively smaller fraction of total mass in obesity, femur BMD, CSA, and SM decline relative to body weight in higher BMI categories.
161	19292617	Femur BMD, CSA, and SM were larger in women with higher BMI, but values scaled in proportion to lean and not to fat or total body mass.
162	19292617	BMD, CSA, and SM vary in proportion to total body lean mass, supporting the view that bones adapt to prevalent muscle loads.
163	19292617	Because lean mass is a progressively smaller fraction of total mass in obesity, femur BMD, CSA, and SM decline relative to body weight in higher BMI categories.
164	19520781	The hormone adiponectin has been shown to be important in maintaining insulin sensitivity throughout the body, whereas potential effects on the placenta have not been assessed.
165	19520781	Adiponectin's role in regulating peripheral insulin responsiveness suggests it may be a factor in maintaining this balance during gestation as well.
166	19520781	Examination of human cytotrophoblast cells revealed that mRNA for both adiponectin receptors, adipoR1 and adipoR2, are abundantly expressed at term.
167	19520781	Treatment of cytotrophoblasts with adiponectin resulted in a significant drop, as assessed by quantitative RT-PCR, in expression for a number of genes involved in the endocrine function of the placenta, including the chorionic gonadotropin subunits, placental lactogen, and some steroidogenic enzymes.
168	19520781	Immunofluorescent staining for connexin 43 and desmoplakin in primary trophoblasts revealed that adiponectin does not inhibit syncytialization of trophoblast cells in culture.
169	20581837	Increasing insulin resistance in the mother maintains nutrient flow to the growing fetus, whereas prolactin and placental lactogen counterbalance this resistance and prevent maternal hyperglycemia by driving expansion of the maternal population of insulin-producing beta cells.
170	20581837	Inhibition of serotonin synthesis by dietary tryptophan restriction or Tph inhibition blocked beta cell expansion and induced glucose intolerance in pregnant mice without affecting insulin sensitivity.
171	20581837	Expression of the G alpha(q)-linked serotonin receptor 5-hydroxytryptamine receptor-2b (Htr2b) in maternal islets increased during pregnancy and normalized just before parturition, whereas expression of the G alpha(i)-linked receptor Htr1d increased at the end of pregnancy and postpartum.
172	21679697	Lactogens (prolactin, placental lactogen and growth hormone) improve β-cell survival via STAT5 activation but the molecular targets are incompletely characterized.
173	21679697	The aim of this study was to examine the effect of human growth hormone (hGH) on mRNAs of fatty acid transport and binding proteins expressed in pancreatic β-cells, and to examine this in relation to β-cell survival after exposure to fatty acids. hGH decreased mRNA levels of FAT/CD36, whereas mRNAs of GPR40, FASN, FABP2, FATP1 and FATP4 were unchanged.
174	21679697	Over-expression of constitutively active STAT5 was able to mimic hGH's suppression of FAT/CD36 expression, whereas dominant negative STAT5 was unable to block the effect of hGH indicating that STAT5 did not bind directly to the FAT/CD36 promoter.
175	21679697	The hGH-mediated suppression of FAT/CD36 mRNA was associated with a decrease in palmitate uptake and fatty acid-induced basal hyper-secretion of insulin resulting in improved glucose-stimulated insulin secretion.
176	21765243	Human placental lactogen (hPL-A) activates signaling pathways linked to cell survival and improves insulin secretion in human pancreatic islets.
177	21765243	Among factors with mitogenic activity on pancreatic β-cells, human placental lactogen (hPL) showed stronger activity when compared to the other lactogen hormones: growth hormone (GH) and prolactin (PRL).
178	21765243	Indeed, the antiapoptotic role of hPL-A was mediated by PI3K, p38 and it was independent by PKA, Erk1/2.
179	21765243	Moreover, hPL-A induced PDX-1 intracellular expression, improving beta cell activity and ameliorating insulin secretion in response to high glucose stimulation.
180	21765243	Human placental lactogen (hPL-A) activates signaling pathways linked to cell survival and improves insulin secretion in human pancreatic islets.
181	21765243	Among factors with mitogenic activity on pancreatic β-cells, human placental lactogen (hPL) showed stronger activity when compared to the other lactogen hormones: growth hormone (GH) and prolactin (PRL).
182	21765243	Indeed, the antiapoptotic role of hPL-A was mediated by PI3K, p38 and it was independent by PKA, Erk1/2.
183	21765243	Moreover, hPL-A induced PDX-1 intracellular expression, improving beta cell activity and ameliorating insulin secretion in response to high glucose stimulation.
184	21823053	The lactogens, human placental lactogen and prolactin, are major stimuli for the adaptation of the endocrine pancreas during gestation.
185	21823053	This review discusses the role of lactogens on glucose homeostasis during pregnancy and proposes a mechanism by which the hormonal control of lactation, led by prolactin, may regulate adipocyte biology, glucose and lipid metabolism, and guard postpartum women against type 2 diabetes.
186	22387044	We investigated how the mRNA expression profile of placental GH2, CSH1 and CSH2 genes and their alternative transcripts correlates with maternal pre-eclampsia (PE) and/or gestational diabetes mellitus (GD).
187	23502141	Hormonal factors such as the growth hormone (GH) and insulin-like growth factor (IGF) signaling system, the human placental lactogen, and insulin play an integral role in early growth.