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At least 1,549 records · Page 86Linked to original sources
PubMed1995

The serotonin-4 receptor agonist cisapride and angiotensin-II exert additive effects on aldosterone secretion in normal man.

In animals and man, serotonin (5-HT) exerts a direct stimulatory action on adrenocortical cells through activation of 5-HT4 receptors. In rats, 5-HT also potentiates the stimulatory effect of angiotensin-II (Ang II) on aldosterone secretion. The aim of the present study was to investigate the effect of concomitant administration of the 5-HT4 receptor agonist, cisapride, and Ang II on aldosterone secretion in normal human subjects. Eight healthy male volunteers pretreated with dexamethasone received, at 1-week intervals in random order and simple blind fashion, the following treatments: 1) a single oral dose of 10 mg cisapride, 2) a single oral dose of placebo, 3) a perfusion of graded doses of Ang II (from 1-4 ng/kg.min), 4) a perfusion of placebo, and 5) a single oral dose of 10 mg cisapride associated with a perfusion of Ang II. The oral doses of cisapride and placebo were also administered after a 3-day period of a low sodium diet (10 mmol/day). Plasma aldosterone levels increased significantly within 90 min after the administration of cisapride without any change in renin levels. The comparison between the net increase in aldosterone production induced by cisapride, Ang II, and cisapride plus Ang II showed that the stimulatory effects of cisapride and Ang II on aldosterone secretion were only additive. Similarly, the increase in plasma aldosterone levels induced by a sodium-restricted diet was just additive with the cisapride-evoked stimulation of aldosterone secretion. These results provide further evidence that the action of 5-HT on glomerulosa cells is mediated through activation of 5-HT4 receptors. The data also indicate that in humans, 5-HT does not potentiate the stimulatory effect of Ang II on aldosterone secretion.

Adult↗
PubMed1995

Blocked growth hormone-releasing peptide (GHRP-6)-induced GH secretion and absence of the synergic action of GHRP-6 plus GH-releasing hormone in patients with hypothalamopituitary disconnection: evidence that GHRP-6 main action is exerted at the hypothalamic level.

GH-releasing peptide (GHRP-6; His-D Trp-Ala-Trp-D Phe-Lys-NH2) is a synthetic compound that releases GH in a specific and dose-related manner through mechanisms and a point of action that are mostly unknown but different from those of GHRH. In man, GHRP-6 is more efficacious than GHRH, and a striking synergistic action on GH release is observed when GHRP-6 and GHRH are administered simultaneously. Based on such a synergistic action, it has been hypothesized that GHRP-6 acts through a double mechanism by actions exerted both at the pituitary and hypothalamic levels. The aim of the present study was 2-fold: 1) to further characterize the mechanism of action and synergistic effects of GHRP-6; and 2) to study its action in patients with hypothalamopituitary disconnection. Twelve patients with different neuroendocrine pathologies leading to a state of hypothalamopituitary disconnection (functional stalk section) and 11 age- and sex-matched normal controls were studied. Each subject underwent 3 tests on separate occasions, being challenged with GHRH (100 micrograms, i.v.), GHRP-6 (90 micrograms, i.v.), or GHRH plus GHRP-6. GH was analyzed as the area under the curve (mean +/- SE, micrograms per L/120 min). In normal subjects GH secretion was 483.7 +/- 99.2 after GHRH, 1434.8 +/- 393.0 after GHRP-6, and 3771.5 +/- 399.6 after GHRH plus GHRP-6; the level of GH secreted after GHRH plus GHRP-6 treatment was significantly (P < 0.05) higher than after the arithmetic sum of GH levels after both compounds administered separately. In the group of patients with hypothalamopituitary disconnection, the level of GH secreted after GHRH was similar to that in controls (423.4 +/- 62.8); however, a complete blockade was observed after GHRP-6 (97.3 +/- 7.9), significantly (P < 0.05) lower than after GHRH as well as lower than the GHRP-6-induced GH release in control subjects (P < 0.01). After GHRH plus GHRP-6, the patients with hypothalamopituitary disconnection showed severely reduced secretion (745.3 +/- 67.6; P < 0.01 vs. controls), a value that was not significantly different from the arithmetic addition of levels produced by both compounds administered separately.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2000

Estrogens exert route- and dose-dependent effects on insulin-like growth factor (IGF)-binding protein-3 and the acid-labile subunit of the IGF ternary complex.

We have previously shown that exogenous estrogens exert route-dependent effects on serum GH and insulin-like growth factor I (IGF-I) levels. IGF-I circulates as a ternary complex with IGF-binding protein-3 (IGFBP-3) and the acid-labile subunit (ALS). It is not known whether IGFBP-3 and ALS in blood are regulated by estrogen and, if so, whether this is also route dependent. In the present study we investigate the effects on IGFBP-3 and ALS of oral and transdermal estrogens (study 1), of different oral estrogen formulations (ethinyl estradiol, conjugated estrogen, and estradiol valerate; study 2), of different estrogen dosages (study 3) in normal postmenopausal women, and of oral estrogen in hypogonadal GH-deficient women (study 4). Administration of oral, but not transdermal, estrogen in normal postmenopausal women significantly decreased serum levels of IGFBP-3 and ALS (P < or = 0.005). The suppressive effects were similar with different oral estrogen formulations, and the degree of suppression increased with estrogen dosage. In hypogonadal GH-deficient women, oral estrogen treatment also significantly reduced IGFBP-3 and ALS (P = 0.02). The changes in IGF-I in each of the four studies paralleled the changes in both IGFBP-3 and ALS. In conclusion, exogenous estrogens suppress serum IGFBP-3 and ALS in a route- and dose-dependent manner, which are in parallel with the effects on serum IGF-I. These actions of oral estrogen are independent of endogenous GH status.

Administration, Cutaneous↗
PubMed2004

Truncated ClC-1 mRNA in myotonic dystrophy exerts a dominant-negative effect on the Cl current.

BACKGROUND: Muscle fiber degeneration and myotonic discharges are the hallmarks of myotonic dystrophy (DM). The molecular basis for the myotonia was recently tied to abnormal splicing of the chloride channel (ClC-1) pre-mRNA, often resulting in UAG premature termination, which leads to decreased channel protein and therefore a reduced resting chloride conductance. METHODS: The authors assessed the functional properties of two commonly occurring DM mRNA splice variants by expression in oocytes. RESULTS: Neither splice variant coded for a functional Cl- channel. Co-injection of alternative splice variants with wild-type ClC-1 cRNA reduced the current density and accelerated channel closure upon repolarization of the membrane. CONCLUSIONS: These data show that the aberrantly spliced chloride channel message exerts a dominant negative effect that may contribute to the development of myotonia.

Alternative Splicing↗
PubMed1989

Control of peripheral glial cell proliferation: enteric neurons exert an inhibitory influence on Schwann cell and enteric glial cell DNA synthesis in culture.

Neuronal membranes from rat dorsal root ganglia provide a mitogenic signal to cultured Schwann cells and it has been suggested this is an important factor in regulating Schwann cell numbers during development. In this study, the influence of enteric neurons on the DNA synthesis of both Schwann cells and enteric glia has been investigated as well as the effect of axonal membrane fractions (axolemma) on enteric glia. The proliferation rate of rat Schwann cells and enteric glia was assessed in culture using [3H]thymidine uptake and autoradiography in combination with immunolabelling to identify cell types. When purified rat Schwann cells were co-cultured with guinea pig enteric neurons, their DNA synthesis rate was reduced compared with control cultures of pure Schwann cells or Schwann cells not close to neurites or neuronal cell bodies. Nevertheless, in accordance with previous findings that sensory neurons stimulate Schwann cell division, these Schwann cells increased their DNA synthesis rate when in contact with neurites from purified guinea pig or adult rat dorsal root ganglion neurons and on exposure to bovine axolemmal fractions. The enteric neurons also suppressed the DNA synthesis of enteric glia in co-cultures of purified enteric neurons and enteric glia, while bovine axolemma stimulated their DNA synthesis. These results indicate that a mitotic inhibitory signal is associated with enteric neurons and can exert its effect on both Schwann cells and enteric glia, and that enteric glia, like Schwann cells, are stimulated to divide by axolemmal fractions. It thus seems possible that during development glial cell numbers in the peripheral nervous system may be controlled by both positive and negative regulators of cell growth.

Animals↗
PubMed1990

Genital ridges exert long-range effects on mouse primordial germ cell numbers and direction of migration in culture.

The functional gametes of all vertebrates first arise in the early embryo as a migratory population of cells, the primordial germ cells (PGCs). These migrate to, and colonise, the genital ridges (GR) during the early organogenesis period, giving rise to the complete differentiating gonad. PGCs first become visible by alkaline phosphatase staining in the root of the developing allantois at 8.5 days post coitum (dpc). At 9.5 dpc they are found in the wall of the hind-gut and, during the following three days, they migrate along the hind-gut mesentery to the dorsal body wall, and then to the genital ridges. By 12.5 dpc, the great majority of PGCs have colonised the genital ridges. During this period the number of PGCs increases from less than 100 to approximately 4000. In a previous paper (Donovan et al. 1986), we showed that 10.5 dpc PGCs can be explanted from the hind-gut mesentery, and will spread and migrate on feeder cell layers. We showed also that the intrinsic ability of PGCs to spread and migrate changes as they colonise the genital ridges. In this paper, we examine extrinsic factors that control PGC behaviour in vitro. Using PGCs taken from 8.5 dpc embryos, at the beginning of their migratory phase, we show that culture medium conditioned by 10.5 dpc genital ridges causes an increase in the number of PGCs in these cultures. We also show that PGCs migrate towards 10.5 dpc genital ridges in preference to other explanted organs. These experiments show that genital ridges exert long-range effects on the migrating population of PGCs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Trithorax regulates multiple homeotic genes in the bithorax and Antennapedia complexes and exerts different tissue-specific, parasegment-specific and promoter-specific effects on each.

The trithorax (trx) gene is required for normal development of the body plan in Drosophila embryos and adults. Mutations in trx cause homeotic transformations throughout the body. Genetic studies suggest that trx encodes a positive regulatory factor required throughout development for normal expression of multiple homeotic genes of the bithorax and Antennapedia complexes (BX-C and ANT-C). To determine how trx influences homeotic gene expression, we examined the expression of the BX-C genes Ultrabithorax, abdominal-A, Abdominal-B and the ANT-C genes Antennapedia, Sex combs reduced and Deformed in trx embryos. We show that trx does indeed exert its effects by positively regulating homeotic gene expression and that its effects on expression of individual homeotic genes are complex: each of the BX-C and ANT-C genes examined exhibits different tissue-specific, parasegment-specific and promoter-specific reductions in their expression. This implies that each of these genes have different requirements for trx in different spatial contexts in order to achieve normal expression levels, presumably depending on the promoters involved and the other regulatory factors bound at each of their multiple tissue- and parasegment-specific cis-regulatory sites in different regions of the embryo. These results also imply that those components of homeotic gene expression patterns for which trx is dispensable, require other factors, possibly those encoded by other trithorax-like genes.

Animals↗
PubMed2002

Drosophila myb exerts opposing effects on S phase, promoting proliferation and suppressing endoreduplication.

Drosophila melanogaster possesses a single gene, Dm myb, that is closely related to the vertebrate family of Myb genes, which encode transcription factors that are involved in regulatory decisions affecting cell proliferation, differentiation and apoptosis. The vertebrate Myb genes have been specifically implicated in regulating the G(1)/S transition of the cell cycle. Dm myb is expressed in all proliferating tissues, but not at detectable levels in endoreduplicating cells. Analysis of loss-of-function mutations in Dm myb revealed a block at the G(2)/M transition and mitotic defects, but did not directly implicate Dm myb function in the G(1/)S transition. We have used the Gal4-UAS binary system of ectopic expression to further investigate the function of Dm myb. Our results demonstrate that depending upon the type of cell cycle, ectopic Dm myb activity can exert opposing effects on S phase: driving DNA replication and promoting proliferation in diploid cells, even when developmental signals normally dictate cell cycle arrest; but suppressing endoreduplication in endocycling cells, an effect that can be overcome by induction of E2F. We also show that a C-terminally truncated DMyb protein, which is similar to an oncogenic form of vertebrate Myb, has more potent effects than the full-length protein, especially in endoreduplicating tissues. This finding indicates that the C terminus acts as a negative regulatory domain, which can be differentially regulated in a tissue-specific manner. Our studies help to resolve previous discrepancies regarding myb gene function in Drosophila and vertebrates. We conclude that in proliferating cells, Dm myb has the dual function of promoting S phase and M phase, while preserving diploidy by suppressing endoreduplication.

Animals↗
PubMed2004

Co-localization with DJ-1 is essential for the androgen receptor to exert its transcription activity that has been impaired by androgen antagonists.

DJ-1 was first identified as a novel candidate of an oncogene product in cooperation with an activated ras, and DJ-1 was later found to be a positive regulator of the androgen receptor (AR) transcription activity that was repressed by PIASxalpha. DJ-1 was also found to be an infertility-related protein that was reduced in rat sperm treated with sperm toxicants that cause infertility in rats. To determine the roles of DJ-1 in the AR function, the effects of several androgen antagonists, some of which had been identified as endocrine-disrupting chemicals, on AR transcription activity and localization of AR and DJ-1 in Cos7 cells were examined. Co-localization of DJ-1 with the AR as dot-like spots in the nucleus was first found in cells that had not been treated with chemicals. Although all of the chemicals tested inhibited AR transcription activity to an average of 25% of that without chemicals, there were two classes affecting the localization of the two proteins; one changes the AR from dot-like spots to diffuse spaces in the nucleus and the other still keeps the AR in the dot-like spots. The localization of DJ-1, on the other hand, was found to be dramatically changed by all of the chemicals, resulting in loss of co-localization with the AR. These results indicate that DJ-1 is an essential factor for the AR to exert its full activity.

Androgen Antagonists↗
PubMed2006

Exertional Rhabdomyolysis during a 246-km continuous running race.

BACKGROUND: To evaluate the effect of continuous, moderate-intensity ultra-endurance running exercise on skeletal muscle and hepatic damage, as indicated by serum enzyme activity measured immediately following the race. METHODS: Thirty-nine runners of the Spartathlon race (a 246-km continuous race from Athens to Sparta, Greece) who managed to complete the race within the 36-h limit participated in this study. Mean finishing time of the study participants was 33.3+/-0.5 h and their average age, height, and body mass were 41+/-1 yr, 174+/-1 cm, and 67.5+/-1.1 kg, respectively. Blood samples, taken a day before and immediately after completion of the race, were assayed for the following variables: creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyltransferase (gamma-GT). RESULTS: A dramatic increase in most of muscle and liver damage indicators was observed. The mean values for CK, LDH, AST, and ALT after the race were 43,763+/-6,764, 2,300+/-285, 1,182+/-165, and 264+/-37 IU.L, respectively. These values were 29,384+/-4,327, 585+/-89, 5,615+/-902, and 1,606+/-331% higher than the corresponding values before the race (P<0.001) for CK, LDH, AST, and ALT, respectively. However, there was not a significant increase in gamma-GT levels. CONCLUSION: Muscle and liver damage indicators were elevated at the highest level ever reported as a result of prolonged exercise, although no severe symptoms that required hospitalization were observed in any of the participants. The data suggest that even moderate-intensity exercise of prolonged duration can induce asymptomatic exertional rhabdomyolysis.

Adult↗
PubMed1993

NC-1300, a proton-pump inhibitor, requires gastric acid to exert cytoprotection in rat gastric mucosa.

Effect of gastric acid suppression on the cytoprotective effect of a single dose of NC-1300 given intragastrically was studied. NC-1300 given intragastrically prevented gastric mucosal damage caused by absolute ethanol in rats in a dose-related manner, while the drug given subcutaneously did not. Pretreatment with NC-1300 given subcutaneously to suppress acid secretion abolished the protective effect of NC-1300 given intragastrically, but not in the presence of 0.1 N HCl. Repeated intragastric administration of NC-1300 for 7 days failed to prevent the ethanol damage. These results suggest that NC-1300 requires gastric acid to exert a protective effect against ethanol in rat gastric mucosa.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2004

Dietary resistant starch alters the characteristics of colonic mucosa and exerts a protective effect on trinitrobenzene sulfonic acid-induced colitis in rats.

The protective effect of a dietary high-amylose cornstarch (HAS) against trinitrobenzene sulfonic acid (TNBS)-induced colitis was examined in rats. Rats were fed a HAS-free basal diet or, a 15% or 30% HAS supplemented diet for 10 d, and then received intracolonic TNBS to induce colitis and fed the respective diets for a further 8 d. HAS ingestion significantly protected colonic injuries as evidenced by lower colonic myeloperoxidase activity. Rats fed the HAS diet showed greater cecal short-chain fatty acid (SCFA) production than those fed the basal diet. Further, just before TNBS administration, HAS ingestion dose-dependently increased fecal and cecal mucin contents, and protein and nucleic acid contents in the colonic mucosa. HAS ingestion also reduced colonic permeability. The protective effect of HAS ingestion on TNBS-induced colitis is perhaps exerted through alterations in colonic mucosa, possibly due to cecal SCFA production.

Animals↗
PubMed2006

Conservation of electromagnetic momentum and radiation forces exerted on left-handed material interfaces.

It is shown that the boundary conditions at left-handed material interfaces cause reversal in the propagation direction of the parallel-to-the-surface electromagnetic energy and momentum fluxes. First-principle examination excludes the possibility of induced surface wave excitation as a way of providing radiation momentum conservation. Thus the imparted net change in electromagnetic momentum should cause a recoil force parallel to the surface, which is unique to left-handed interfaces. The shear force exerted on a left-handed material interface is computed. The magnitude of this force is found detectable by experiments.

Journal Article↗
PubMed2003

Pharmacological levels of copper exert toxic effects in Caco-2 cells.

Copper might be toxic to human intestinal cells because of its ability to catalyze the formation of free radicals. The aim of the present study was to quantify toxicological effects of increasing copper concentrations in preconfluent, colonic cancerous cells as well as in postconfluent, differentiating Caco-2 cells. Our results indicate that postconfluent cells might be more sensitive to copper toxicity. A significant rise of lactate dehydrogenase (LDH) release (150 microM or above) and decrease of cell proliferation (100 microM or above) with increasing copper levels was found, as compared to the control. To the contrary, preconfluent cells were not significantly affected by copper (LDH release) or, if so, only at a concentration of 250 microM (proliferation). Loss of viability and morphological changes, including loss of adherence and cell rounding, were visible after incubation with 250 microM copper in both groups. Superoxide dismutase (SOD) activities were not affected by copper. Glutathione peroxidase (GSH-Px) and catalase activities were higher in copper-treated cells, especially in the postconfluent ones (nevertheless, the results were not significant because of high standard deviations). In conclusion, we demonstrated that copper exerts intracellular, toxicological effects on both groups of Caco-2 cells, although the effects seem to be more evident in the postconfluent (enterocytelike) group. Risk assessment, especially for high concentrations, might be of special interest.

Antioxidants↗
PubMed2006

Transplantation of human neural stem cells exerts neuroprotection in a rat model of Parkinson's disease.

Neural stem cells (NSCs) possess high potencies of self-renewal and neuronal differentiation. We explored here whether transplantation of human NSCs cloned by v-myc gene transfer, HB1.F3 cells, is a feasible therapeutic option for Parkinson's disease. In vivo, green fluorescent protein-labeled HB1.F3 cells (200,000 viable cells in 3 microl of PBS) when stereotaxically transplanted (same-day lesion-transplant paradigm) into the 6-hydroxydopamine-lesioned striatum of rats significantly ameliorated parkinsonian behavioral symptoms compared with controls (vehicle, single bolus, or continuous minipump infusion of trophic factor, or killed cell grafts). Such graft-derived functional effects were accompanied by preservation of tyrosine hydroxylase (TH) immunoreactivity along the nigrostriatal pathway. Grafted HB1.F3 cells survived in the lesioned brain with some labeled with neuronal marker mitogen-activated protein 2 and decorated with synaptophysin-positive terminals. Furthermore, endogenous neurogenesis was activated in the subventricular zone of transplanted rats. To further explore the neuroprotective mechanisms underlying HB1.F3 cell transplantation, we performed cell culture studies and found that a modest number of HB1.F3 cells were TH and dopamine and cAMP-regulated phosphoprotein 32 positive, although most cells were nestin positive, suggesting a mixed population of mature and immature cells. Administration of the HB1.F3 supernatant to human derived dopaminergic SH-SY5Y cells and fetal rat ventral mesencephalic dopaminergic neurons protected against 6-hydroxydopamine neurotoxicity by suppressing apoptosis through Bcl-2 upregulation, which was blocked by anti-stem cell factor antibody alone, the phosphatidylinositol 3-kinase/Akt inhibitor LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one] alone, or a combination of both. These results suggest that HB1.F3 cell transplantation exerts neuroprotective effects against dopaminergic depletion in vitro and in vivo because of trophic factor secretion and neuronal differentiation.

Animals↗
PubMed2004

The force exerted by the membrane potential during protein import into the mitochondrial matrix.

The force exerted on a targeting sequence by the electrical potential across the inner mitochondrial membrane is calculated on the basis of continuum electrostatics. The force is found to vary from 3.0 pN to 2.2 pN (per unit elementary charge) as the radius of the inner membrane pore (assumed aqueous) is varied from 6.5 to 12 A, its measured range. In the present model, the decrease in force with increasing pore width arises from the shielding effect of water. Since the pore is not very much wider than the distance between water molecules, the full shielding effect of water may not be present; the extreme case of a purely membranous pore without water gives a force of 3.2 pN per unit charge, which should represent an upper limit. When applied to mitochondrial import experiments on the protein barnase, these results imply that forces between 11 +/- 2 pN and 13.5 +/- 2.5 pN catalyze the unfolding of barnase in those experiments. A comparison of these results with unfolding forces measured using atomic force microscopy is made.

Animals↗
PubMed1997

C-type natriuretic peptide exerts stimulatory effects on the corticotropin-releasing hormone-induced secretion of hormones in normal man.

C-type natriuretic peptide and atrial natriuretic peptide have been reported to bind to distinct receptors and to exert opposing effects on different systems. Although it is known that atrial natriuretic peptide inhibits the corticotropin-releasing hormone-stimulated hormone release in man, the corresponding action of C-type natriuretic peptide has so far not been characterized. We investigated the effects of 30-min infusions of 150 and 300 micrograms C-type natriuretic peptide on adrenocorticotropin, cortisol, and prolactin release stimulated by 100 micrograms corticotropin-releasing hormone and on cardiovascular parameters in 8 healthy male volunteers. Compared with placebo, 300 micrograms C-type natriuretic peptide significantly (P < 0.05) enhanced the stimulation of cortisol (area under curve (arbitrary units): 520 +/- 35 vs 651 +/- 55) and prolactin (area under curve: 29 +/- 3 vs 37 +/- 5). Adrenocorticotropin levels were increased, but the differences did not reach statistical significance (maximum increment: 27 +/- 4 vs 36 +/- 2 pg/ml). C-type natriuretic peptide at a dose of 150 micrograms had no clear effect on these hormones and C-type natriuretic peptide also produced no cardiovascular or subjective effects. Our data suggest stimulatory effects of C-type natriuretic peptide on corticotropin-releasing hormone-induced hormone release and offer further evidence for a complex role of different natriuretic peptides in endocrine regulation.

Adrenocorticotropic Hormone↗
PubMed2004

Body mass reduction markedly improves muscle performance and body composition in obese females aged 61-75 years: comparison between the effects exerted by energy-restricted diet plus moderate aerobic-strength training alone or associated with rGH or nandrolone undecanoate.

OBJECTIVE: To investigate the effectiveness of a body mass reduction programme entailing diet caloric restriction and moderate physical activity with or without supplementary treatment with recombinant (r) GH or steroids to improve body composition and muscle performance in severely obese women aged 61-75 years. METHODS: Twenty women were randomly assigned to one of three groups: body mass reduction alone; body mass reduction plus rGH; body mass reduction plus nandrolone undecanoate. Body composition, isotonic muscle strength and anaerobic power output during jumping were determined before and after the 3-week period. RESULTS: Whatever the experimental group considered, body mass (P<0.01), body mass index (P<0.05) and fat mass (P<0.05) decreased significantly, whereas muscle strength and power increased significantly (P<0.05) after the intervention. CONCLUSION: Small body mass reductions after 3 weeks of energy-restricted diet combined with moderate aerobic and strength exercise are associated with significant improvements in upper and lower limb muscle strength and power and reduction of fat mass in severely obese women aged 61-75 years. Although the association of rGH or nandrolone undecanoate does not appear to exert additional effects on body composition and muscle performance attained by body mass reduction alone, further additional studies with larger study groups, different dosages and more prolonged periods are required for definitive conclusions to be drawn.

Aged↗