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Biomedical subjects

A Goulding

Publications and source records attributed to A Goulding.

At least 55 records · Page 3Linked to original sources
PubMed1996

DEXA supports the use of BMI as a measure of fatness in young girls.

OBJECTIVE: To examine the relationship of body fat mass measured by dual energy X-ray absorptiometry (DEXA) to BMI in young girls, according to age and normative BMI percentile groupings. DESIGN: Cross-sectional observation study. SETTING: Dunedin, an urban town in the South Island of New Zealand. SUBJECTS: 196 healthy Caucasian girls aged 4-16 y. MEASUREMENTS: Body weight, height and BMI, total fat mass and % body fat (by DEXA). RESULTS: Our BMI percentile standard groupings were < 5 centile (n = 7); 5-50 centile (n = 71); 51-75 centile (n = 50); 76-90 centile (n = 42); 91-95 centile (n = 12); > 95 centile (n = 14). In this whole population sample DEXA-derived fat mass correlates well with BMI (n = 0.934) indicating that BMI accounts for 87.2% of the variance in body fat mass. However, at the extremes of BMI the association is weaker. A nomogram for predicting DEXA fat mass from BMI in girls is presented. CONCLUSION: Because DEXA-derived fat mass correlates well with BMI throughout the 'normal' range of BMI (5-95th centiles) our study supports the usefulness of BMI as a simple measure of fatness in girls. Children with BMI values outside the normal BMI range may benefit from more exact body composition assessment using DEXA.

Absorptiometry, Photon↗
PubMed1994

Tamoxifen and norethisterone: effects on plasma cholesterol and total body calcium content in the estrogen-deficient rat.

It is important that drugs which are used to protect bone from the osteoporotic effects of estrogen deficiency should not affect plasma lipids adversely. Effects of a) norethisterone acetate and b) tamoxifen citrate on plasma cholesterol and on bone conservation in rats with normal plasma 17B-estradiol and in rats made estrogen-deficient with the LHRH agonist, buserelin are reported. Tamoxifen halved total plasma cholesterol (p < 0.01), whereas norethisterone did not lower plasma cholesterol. Furthermore tamoxifen fully protected bone from estrogen-deficiency osteopenia whereas norethisterone conserved bone less well. Reductions in cholesterol elicited by tamoxifen were similar in estrogen-deficient rats and in rats with normal ovarian function. This is the first report in the rat that tamoxifen has lipid-lowering actions. It is suggested the rat may be useful for future investigations of the lipid-lowering mechanisms of tamoxifen.

Animals↗
PubMed1993

Low follicular oestrogen levels in New Zealand women consuming high fibre diets: a risk factor for osteopenia?

AIMS: To study effects of anthropometry, diet and exercise on plasma 17 beta-oestradiol concentrations in healthy premenopausal women. METHODS: Fifty-five healthy female volunteers aged 19-29 (Mean (SD) = 22.2 (2.6) years) were studied. Anthropometric measurements were made, food intakes were estimated using a food frequency questionnaire, physical activity was assessed, menstrual histories were taken and blood 17 beta-oestradiol values were measured in the follicular and luteal phases of the menstrual cycle. RESULTS: Adiposity and dietary fat intake did not influence circulating plasma 17 beta-oestradiol but dietary fibre intake was negatively correlated with both follicular (r = -0.43, p < 0.001) and luteal (r = -0.28, p < 0.05) 17 beta-oestradiol concentrations. Follicular oestradiol values were abnormally low in 53% of the population. Subjects with high fibre intakes (> or = 25 g fibre daily) had significantly lower concentrations of 17 beta-oestradiol in the follicular phase of the menstrual cycle (p < 0.01). Physical activity was similar in groups consuming high and low fibre diets. Subjects with oligomenorrhoea or amenorrhoea (n = 7) had higher fibre intakes/energy (p < 0.05) than subjects with eumenorrhoea (n = 48). CONCLUSION: Our study suggests that healthy New Zealand women of premenopausal age have lower 17 beta-oestradiol levels on high fibre diets than on low fibre diets. Because hypoestrogenism is a known risk factor for osteoporosis we propose that high fibre intakes may influence bone mass adversely and be a risk factor for osteoporosis. The effects of high fibre intakes on bone mass warrant further investigation.

Adult↗
PubMed1993

Flutamide-mediated androgen blockade evokes osteopenia in the female rat.

Androgens are believed to play a role in building and maintaining bone in the female, as well as in the male. The antiandrogen drug flutamide inhibits responses to androgens from both the gonads and the adrenals. Antiandrogens prevent androgens stimulating bone cell proliferation and differentiation in vitro, but effects of androgen blockade on bone metabolism in vivo have not been tested. The present study was undertaken to determine whether androgen blockade with flutamide (15 mg/kg body weight orally daily) would influence bone turnover or bone composition (1) in female rats with intact ovaries and (2) in rats made estrogen-deficient with the luteinizing hormone releasing hormone (LHRH) agonist, buserelin (25 micrograms/kg body weight per day SC). Four groups of rats with 45Ca-labeled skeletons were studied for 4 weeks: group A, placebo; group B, buserelin; group C, flutamide; group D, flutamide+buserelin. Total-body calcium values (mean +/- SD) were (mg) 2007 +/- 109, 1779 +/- 138 (P < 0.01 versus group A), 1818 +/- 140 (P < 0.01 versus group A), and 1690 +/- 75 (P < 0.01 versus group A) in groups A-D, respectively. Thus both buserelin and flutamide induced osteopenia. Skeletal 45Ca changes suggested buserelin-mediated estrogen deficiency bone loss was due to increased bone resorption, but flutamide-mediated androgen deficiency bone thinning was caused principally by reduced bone formation. These findings support the view that androgens play an important role in preserving bone mass in the female rat. Importantly, adequate estrogen status did not compensate for flutamide-mediated osteopenia.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgens↗
PubMed1993

Norethindrone acetate only partially protects the skeleton of rats treated with the LHRH agonist buserelin from oestrogen-deficiency osteopaenia.

In women with endometriosis there is concern that therapeutic use of LH-releasing hormone (LHRH) analogues, to lower ovarian oestrogen production and control endometrial hyperplasia, leads to unwanted oestrogen-deficiency bone loss. We have developed an animal model of this LHRH-mediated oestrogen-deficiency bone loss in the rat, using buserelin. The aim was to use this model to determine whether the progestogen, norethindrone acetate, could counter oestrogen-deficiency bone loss associated with prolonged treatment with the LHRH agonist buserelin. Four groups of animals which had their bones labelled with 45Ca were studied for 4 weeks: group A, control; group B, buserelin treated; group C, norethindrone acetate treated; group D, norethindrone acetate+buserelin treated. Buserelin was given daily (19.2 pmol/kg body wt); norethindrone was given orally three times/week (1.47 mumol/kg body wt). Bone resorption was monitored by measuring the urinary excretion of hydroxyproline and 45Ca and bone 45Ca content. Buserelin-treated rats developed similarly depressed plasma oestradiol-17 beta values in the presence and absence of progestogen, and both groups given buserelin had significantly smaller uteri than controls or rats given norethindrone without buserelin. However, norethindrone did not prevent buserelin-mediated increases in bone resorption. At the end of the study total body calcium values (mean +/- S.D.) in the four groups were (mg) respectively; 2594 +/- 123; 2260 +/- 92 (P < 0.001 compared with controls); 2616 +/- 221; 2415 +/- 130 (P < 0.02 compared with controls). Rats given norethindrone and buserelin in combination had higher values (P < 0.02) than animals given buserelin alone, but significantly less total body calcium than controls (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Tamoxifen in the rat prevents estrogen-deficiency bone loss elicited with the LHRH agonist buserelin.

In young women chronic use of luteinizing hormone releasing hormone (LHRH) agonists such as buserelin to treat endometriosis leads to estrogen-deficiency bone loss. Tamoxifen citrate is an estrogen agonist/antagonist which protects the skeleton from osteopenia when ovarian hormones are depleted. The present study was undertaken to determine whether tamoxifen citrate (20 mg/kg body wt/week s.c.) could prevent the osteopenic effect of buserelin (25 micrograms/kg body wt/day s.c.). Four groups of rats with 45Ca-labelled bones were studied for 4 weeks: group A--placebo controls; group B--buserelin; Group C--tamoxifen; group D--buserelin+tamoxifen. Bone resorption was monitored by measuring the urinary excretion of 45Ca and hydroxyproline. Interestingly buserelin lowered both blood 17 beta-estradiol values and uterine weights in the presence and absence of tamoxifen. However, tamoxifen slowed bone breakdown and inhibited the bone-thinning effects of buserelin. Total body calcium values (mg; means +/- S.D.) were: 2227 +/- 137; 1926 +/- 124; 2233 +/- 94 and 2268 +/- 163, in groups A to D respectively. Osteopenia was thus present only in group B (P less than 0.001). Because tamoxifen inhibits estrogen-deficiency bone loss in buserelin-treated rats without depressing the hypoestrogenic actions of this LHRH-agonist, we suggest that use of tamoxifen to protect the skeleton during LHRH-agonist therapy in young women should be explored. Tamoxifen citrate might also help to prevent postmenopausal osteoporosis.

Animals↗
PubMed1991

Lactose malabsorption and calcium intake as risk factors for osteoporosis in elderly New Zealand women.

OBJECTS: to evaluate the prevalence of lactose malabsorption and to assess dietary calcium intake, in elderly New Zealand women with hip fractures, in age matched case controls without hip fractures drawn from general practice, and in healthy young women. METHODS: lactose malabsorption was assessed by measuring breath hydrogen after a 50 g oral lactose tolerance test. Dietary calcium was estimated from a food frequency questionnaire. RESULTS: the elderly fracture cases (n = 15), and their elderly controls (n = 16), showed a similar (60% and 63% respectively), but significantly higher prevalence (p less than 0.001), of lactose malabsorption than young women (12%, n = 50). Dietary calcium intake was similar in lactose absorbers and malabsorbers. CONCLUSIONS: malabsorption of lactose occurs commonly in elderly New Zealand women but is scarce in young adults. A high prevalence of lactose malabsorption may be a risk factor for exacerbation of type II osteoporosis in the elderly.

Adolescent↗
PubMed1991

Preventive effects of clomiphene citrate on estrogen-deficiency osteopenia elicited by LHRH agonist administration in the rat.

The estrogen agonist and antagonist clomiphene citrate has been shown to prevent bone loss induced by ovariectomy in the rat. In young women estrogen-deficiency bone loss is a clinical problem associated with the use of luteinizing hormone releasing hormone (LHRH) agonists, such as buserelin, to treat endometriosis. The aim of this study was to determine whether clomiphene citrate (10 mg/kg body weight per week orally) would prevent the osteopenic effect of buserelin (25 micrograms/kg body weight per day SC) in the rat. Four groups of animals with 45Ca-labeled skeletons were studied for 4 weeks: group A, placebo controls; group B, buserelin; group C, clomiphene; and group D, buserelin + clomiphene. Bone resorption was monitored by measuring the urinary excretion of 45Ca and hydroxyproline. Clomiphene slowed bone breakdown and inhibited the osteopenic effect of buserelin. Total-body calcium values (mean +/- SD) were (mg) 2635 +/- 181, 2267 +/- 85, 2566 +/- 126, and 2624 +/- 77 in groups A to D, respectively. Osteopenia was present only in group B (P less than 0.001). Interestingly buserelin lowered blood 17 beta-estradiol and uterine weights to a similar extent in the presence and absence of clomiphene. Because clomiphene inhibited estrogen-deficiency bone loss in buserelin-treated rats without depressing the hypoestrogenic action of this LHRH agonist, it is suggested that the use of clomiphene to protect the skeleton during LHRH agonist therapy of endometriosis warrants further study.

Animals↗
PubMed1991

17 beta-estradiol protects rats from osteopenia associated with administration of the luteinising hormone releasing hormone (LHRH) agonist, buserelin.

Bone loss associated with sustained administration of luteinising hormone releasing hormone (LHRH) agonists, such as buserelin, is attributed to estrogen deficiency. However, the possibility that the LHRH agonists themselves may contribute to the pathogenesis of bone thinning, has not been ruled out. The aim of the present study was to determine whether or not oral 17 beta-estradiol (300 micrograms/kg body wt/week) would fully prevent the osteopenic effect of buserelin (25 micrograms/kg body wt/day s.c.) in the rat. Four groups of animals with 45Ca-labelled skeletons were studied for 4 weeks: group 1, placebo controls; group 2, 17 beta-estradiol; group 3, buserelin; group 4, 17 beta-estradiol + buserelin. Buserelin alone lowered blood estradiol concentrations, increased bone resorption and reduced femur and total body calcium and 45Ca values. Total body calcium values (means +/- SD) were: (mg) 3405 +/- 176; 3250 +/- 282; 2813 +/- 133; 3156 +/- 452 in groups 1 to 4, respectively. Significant osteopenia was present only in group 3 (P less than 0.001). These results support the view that buserelin-mediated bone loss is due to estrogen deficiency. They do not indicate that LHRH agonists per se, play any role in causing bone thinning.

Animals↗
PubMed1990

Buserelin-mediated osteoporosis: effects of restoring estrogen on bone resorption and whole body calcium content in the rat.

In the rat, prolonged administration of the luteinizing, hormone-releasing hormone agonist buserelin (25 micrograms/kg body wt/day s.c.) lowers blood estradiol, raises bone resorption, and induces osteopenia. The present study was undertaken to determine whether withdrawal of buserelin normalizes blood estradiol, slows bone resorption, and corrects buserelin-mediated osteopenia. Four groups of female rats with 45Ca-labeled bones were studied: group 1A received 0.2 ml saline s.c. daily for 4 weeks; group 2A received 0.2 ml buserelin s.c. daily for 4 weeks; group 1B received 0.2 ml saline s.c. daily for 8 weeks; group 2B received 0.2 ml buserelin s.c. daily for 4 weeks followed by 0.2 ml saline s.c. daily for 4 weeks. Bone resorption was monitored by measuring urinary 45Ca and hydroxyproline. The rats in groups 1A and 2A were killed after 4 weeks and those in groups 1B and 2B after 8 weeks. The mineral contents of the femoral bones and the whole skeletons were measured. Buserelin lowered blood estradiol, elevated urinary 45Ca and urinary hydroxyproline, and lowered femur and total body calcium and 45Ca in group 2A vs. 1A (P less than 0.05). By contrast all these measurements became similar in groups 2B and 1B. Thus, osteopenia generated by a 4-week period of buserelin-mediated hypo-estrogenism is reversible by withdrawing buserelin for 4 weeks. Consequently, buserelin administration and withdrawal may be used to study effects of inducing and reversing estrogen-deficiency bone loss in the rat.

Animals↗
PubMed1990

Effects of clomiphene and tamoxifen in vivo on the bone-resorbing effects of parathyroid hormone and of high oral doses of calcitriol (1,25(OH)2D3) in rats with intact ovarian function consuming low calcium diet.

Two experiments were undertaken to study the abilities of clomiphene citrate (20 mg/kg body wt/wk s.c.) and tamoxifen citrate (20 mg/kg body wt/wk s.c.) to slow bone resorption mediated by (a) endogenous parathyroid hormone (PTH) and (b) exogenous calcitriol (1,25(OH)2D3) in vivo in rats with intact ovarian function. Groups of rats with 45Ca-labelled bones were fed a low-calcium (0.01% Ca) diet to stimulate secretion of PTH. Neither clomiphene nor tamoxifen showed the mobilization of 45Ca from femoral bone or prevented the reduction in bone calcium induced by feeding this diet. Moreover these drugs did not depress the urinary excretion of 45Ca or hydroxyproline. These observations indicated that clomiphene and tamoxifen did not inhibit PTH-mediated bone resorption. Administering calcitriol (50 ng/day) orally for 14 days raised plasma calcium, increased urinary 45Ca and its specific activity and decreased femur 45Ca: all these responses were similar in animals receiving calcitriol alone and calcitriol with clomiphene or tamoxifen. The femur 45Ca values (dpm X 10(-3) were: (mean +/- SD, n = 8) placebo, 1901 +/- 127; 1,25(OH)2D3, 1727 +/- 96**; clomiphene + 1,25(OH)2D3, 1694 +/- 93**; tamoxifen + 1,25(OH)2D3, 1664 +/- 61**. (** = P less than 0.01). Thus neither clomiphene nor tamoxifen prevented calcitriol-mediated bone resorption in vivo in the rat.

Animals↗
PubMed1990

Fasting and 24-h urinary sodium/creatinine values in young and elderly women on low-salt and salt-supplemented regimens.

A high sodium intake is a risk factor for both hypertension and osteoporosis. High-salt diets cause calciuresis and may influence blood pressure (BP) by stimulating calcium-regulating hormones and augmenting intracellular calcium concentrations. Urinary calcium rises in parallel with urinary sodium. However, aging may influence the rate of excretion of a dietary sodium load. This study compares sodium/creatinine (Na/Cr) values in 2-h urines collected after an overnight fast (12 h) with values obtained in 24-h urines from normotensive women aged (a) 19-23 years (n = 6) and (b) 65-70 years (n = 9) who were consuming either 70 mmol of Na/day [low-sodium regimen (LSR)] or 170 mmol of Na/day [supplemental sodium regimen (SSR)]. Young and elderly women excreted similar amounts of sodium per 24-h period. The 24-h urinary sodium excretion matched dietary sodium input appropriately on LSR and SSR, and SSR raised calcium excretion by 30%. However, whereas in the young women Na/Cr values were similar in fasting and 24-h collections on both LSR and SSR, these values were higher in 24-h than in fasting urines on SSR in the elderly women. We attribute this response to temporal differences in urinary sodium excretion associated with aging. We conclude that assessing sodium excretion from fasting urinary sodium measurements may underestimate total sodium loss (and hence calcium loss) in subjects on a stable sodium intake, particularly in the elderly.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Fasting urinary calcium/creatinine and hydroxyproline/creatinine values in young women with amenorrhoea and in matched eumenorrhoeic controls.

The present study was undertaken to compare fasting urinary calcium/creatinine (Ca/Cr) and hydroxyproline/creatinine (HP/Cr) values in young amenorrhoeic women with those of age and weight-matched menstruating women and to see whether restoration of menstruation would influence values. Thirty amenorrhoeic patients were matched with 30 controls. Higher Ca/Cr (0.393 (SD 0.213) vs 0.142 (0.89), p less than 0.001) and HP/Cr (0.025 (0.005) vs 0.020 (0.007), p less than 0.005) values were found in patients with hyperprolactinaemia or hypothalamic dysfunction associated with weight loss, anorexia nervosa or excessive exercise (n = 20), suggesting excessive bone loss in these amenorrhoeic patients, who are frequently oestrogen deficient. Furthermore when 9 amenorrhoeic patients with hypothalamic dysfunction became eumenorrhoeic their urinary Ca/Cr values fell (p less than 0.02). However, amenorrhoeic patients with polycystic ovaries (n = 10) had similar Ca/Cr and HP/Cr values as their controls. It is therefore probable that amenorrhoeic patients with polycystic ovaries are not at risk of osteopenia. The present findings suggest measurements of fasting urinary Ca/Cr and HP/Cr values are likely to prove useful in identifying patients with amenorrhoea who are rapidly losing bone, and in assessing their responses to therapy.

Adult↗
PubMed1989

Estrogens and progestogens conserve bone in rats deficient in calcitonin and parathyroid hormone.

To examine the abilities of estrogens and progestogens to slow bone resorption and conserve bone in ovariectomized rats deficient in calcitonin (CT) or parathyroid hormone (PTH), nine groups of animals with 45Ca-labeled bones were studied for 12 wk. Rats were thyroidectomized (TX), parathyroidectomized (PTX), or given sham neck operations (Sham) and treated orally with either estrogen, 300 micrograms 17 beta-estradiol.kg body wt-1.wk-1; progestogen, 500 micrograms norethisterone acetate.kg body wt-1.wk-1; or placebo (Plac). The TX rats had parathyroid autografts and thyroxine replacement. In all surgical groups, estradiol (E2) and norethindrone (Nor) slowed urinary 45Ca excretion and conserved bone (P less than 0.001). However E2 lowered urinary hydroxyproline more than Nor. Total body Ca values (mg +/- SD) were Sham + Plac, 3,079 +/- 201; Sham + E2, 3,886 +/- 335; Sham + Nor, 3,567 +/- 459; TX + Plac, 3,123 +/- 159; TX + E2, 3,869 +/- 235; TX + Nor, 3,540 +/- 422; PTX + Sham, 3,067 +/- 249; PTX + E2, 3,775 +/- 414; PTX + Nor, 3,635 +/- 467. Importantly, E2 and Nor conserved bone as effectively in TX and PTX groups as in Sham rats, although the PTX rats had slower bone resorption and lower plasma 1,25-dihydroxyvitamin D values (P less than 0.001) than groups with intact parathyroids. We conclude that the effects of estrogens and progestogens to slow bone resorption and conserve bone are independent of CT and PTH. These findings appear relevant to the pathogenesis and treatment of postmenopausal osteoporosis.

Animals↗
PubMed1989

A new way to induce oestrogen-deficiency osteopaenia in the rat: comparison of the effects of surgical ovariectomy and administration of the LHRH agonist buserelin on bone resorption and composition.

Prolonged administration of LHRH agonist suppresses pituitary gonadotrophin secretion, thereby lowering blood oestrogen. This study was undertaken to compare the osteopaenic effects of bilateral ovariectomy and chronic administration of the LHRH agonist, buserelin, in the rat. Four groups of animals which had their skeletons labelled with 45Ca were studied for 4 weeks. Group 1 underwent a sham-ovariectomy, group 2 were surgically ovariectomized, group 3 were given buserelin by daily s.c. injection and group 4 were given a continuous infusion of buserelin by osmotic minipump. Plasma concentrations of oestradiol were measured weekly. Bone resorption was assessed by measuring the urinary excretion of 45Ca and hydroxyproline and determining bone 45Ca content. Ovariectomy and buserelin treatments lowered blood oestradiol, increased biochemical indices of bone resorption and decreased femur and total body calcium and 45Ca values. The degree of oesteopaenia elicited by ovariectomy and buserelin treatment was similar. Bone responses to s.c. buserelin and to continuous buserelin infusion were alike. We attribute evidence of increases in bone resorption and induction of osteopaenia with buserelin treatment to hypo-oestrogenism. We have shown for the first time by bone analysis that buserelin induces osteopaenia as effectively as bilateral ovariectomy. This appears to be the first demonstration in the rat that long-term administration of LHRH agonist influences bone. Administration of buserelin provides a new way of inducing oestrogen-deficiency osteopaenia in the rat without removing the ovaries.

Animals↗