Biomedical subjects

L Limlomwongse

Publications and source records attributed to L Limlomwongse.

At least 19 recordsLinked to original sources

PubMed2001

Study of acute pharmacologic effects of prolactin on calcium and water transport in the rat colon by an in vivo perfusion technique.

We investigated the acute effect of intraperitoneally administered prolactin on calcium and water transport in colon of sexually mature female Wistar rats using an in vivo perfusion technique. Test solution containing (in mM) NaCl, 100; KCl, 4.7; MgSO4, 1.2; CaCl2, 20; D-glucose, 11; sodium ferrocyanide (Na4Fe(CN)6), an index of net water transport, 20; and 0.7 (microCi 45CaCl2 (1 Ci = 37 GBq) was perfused througth the 8-cm colonic loop for 60 min at perfusion rates of 0.5 or 1.0 mL x min(-1). Calcium and water transport was also studied under a no flow condition to stimulate the condition often found in the colon by in vivo ligated colonic loop for 30 min. Control results showed no correlation between calcium transport and water flux. Flow of luminal solution at 0.5 and 1.0 mL x min(-1) was found to reverse net calcium absorption from 0.04+/-0.01 nmol x g(-1) dry weight x h(-1) to net calcium secretion of 0.04+/-0.04 and 0.9+/-0.02 nmol x g(-1) dry weight x h(-1), respectively. Neither 0.4, 0.6, nor 1.0 mg x kg(-1) prolactin had any effect on calcium fluxes in the colon. On the other hand, at a perfusion rate of 1 mL x min(-1), 0.4 mg x kg(-1) prolactin significantly decreased net water absorption from 3.86+/-0.90 to 0.88+/-0.64 mL x g(-1) dry weight x h(-1) (P < 0.001), and the higher doses of 0.6 and 1.0 mg x kg(-1) prolactin reversed net water absorption to net water secretion of 2.20+/-0.63 and 2.33+/-0.89 mL x g(-1) dry weight x h(-1), respectively (P < 0.001). The stimulatory effect of prolactin on water transport was completely abolished by reducing the perfusion rate from 1.0 mL x min(-1) to zero. The stimulatory effect of prolactin on water secretion at perfusion rate of 1.0 mL x min(-1) was also abolished when luminal [Na+] was reduced from 180 to 80 mM. We concluded that, unlike in the small intestine, calcium fluxes in the colon are not related to water transport and did not respond at all to prolactin. Water transport, on the other hand, was reversed from net absorption to secretion by prolactin. We propose that this prolactin-induced water secretion is probably mediated by recycling of luminal sodium in the vicinity of tight junctions.

Animals↗

PubMed2001

Prolactin directly stimulates transcellular active calcium transport in the duodenum of female rats.

Prolactin has been postulated to be a novel calcium-regulating hormone during pregnancy and lactation. It stimulates both passive and active duodenal calcium transport in several experimental models. Our study was performed on sexually mature female Wistar rats (200-250 g) to study the direct action of prolactin on calcium transport in the duodenum using the Ussing chamber technique. To evaluate the effect of prolactin on total calcium transport in the duodenum, we intraperitoneally injected rats with 0.4, 0.6, and 0.8 mg/kg prolactin. The total calcium transport was divided into voltage-dependent, solvent drag-induced, and transcellular active fluxes by applying short-circuit current and by mucosal glucose replacement with mannitol. The effect of prolactin on each flux was studied separately. Finally, to evaluate the direct action of prolactin on duodenal transcellular active flux, we directly exposed duodenal segments to prolactin that had been added to the serosal solution with or without calcium transport inhibitors. We found that 0.6 and 0.8 mg/kg prolactin ip significantly increased the total mucosa-to-serosa calcium flux from the control value (nmol x hr(-1) x cm(-2)) of 34.53+/-6.81 to 68.07+/-13.53 (P < 0.05) and 84.43+/-19.72 (P < 0.01), respectively. Prolactin also enhanced the solvent drag-induced calcium flux and transcellular active calcium flux, but not the voltage-dependent calcium flux. The duodenal segments directly exposed to 200, 400, and 800 ng/mL prolactin showed a significant increase in the transcellular active calcium absorption in a dose-dependent manner, i.e., from the control value (nmol x hr(-1) x cm(-2)) of 2.94+/-0.47 to 5.45+/-0.97 (P < 0.01), 8.09+/-0.52 (P < 0.001), and 18.42+/-2.92 (P < 0.001), respectively. Its direct action was inhibited by mucosal exposure to 50 microM lanthanum chloride, a calcium transporter protein competitor, and serosal exposure to 0.1 mM trifluoperazine, a Ca2+-ATPase inhibitor. These studies demonstrate that the duodenum is a target organ of prolactin, which enhances transcellular active calcium transport.

Animals↗

PubMed2000

Changes in the regulation of calcium metabolism and bone calcium content during growth in the absence of endogenous prolactin and during hyperprolactinemia: a longitudinal study in male and female Wistar rats.

Since endogenous prolactin has been shown to enhance food consumption, calcium absorption, and bone calcium turnover in the pregnant rat, the role of endogenous prolactin in the regulation of calcium metabolism was investigated in 3-day balance studies of female Wistar rats from the age of 3 to 11 weeks. The study was divided into two parts. In part I, calcium metabolism in males and females was compared. In part II, 3-week old female rats were divided into 5 groups: (i) control animals receiving 0.9% NaCl; (ii) animals receiving 6 mg bromocriptine/kg/day (- PRLendo group); (iii) animals receiving 2.5 mg ovine prolactin/kg/day (+PRLexo); (iv) sham-operated animals receiving 0.9% NaCl, and (v) animals with two extra pituitaries implanted under the renal capsule, receiving 0.9% NaCl (AP group). Results showed that rapid growth occurred between 3 and 6 weeks with maximum fractional calcium absorption and calcium retention at 5 weeks of age in both sexes. The data also showed a physiological significance of endogenous prolactin in enhancing calcium absorption and retention in 5 week old rats. In an absence of prolactin, peak calcium absorption was delayed in 7-week old animals, and vertebral calcium content of 11-week old animals was reduced by 18%. Hyperprolactinemia in the AP group was found to enhance fractional calcium absorption and calcium retention at 7, 9, and 11 weeks and increased the femoral calcium content by 16%. It could be concluded that a physiological role of prolactin is the stimulation of calcium absorption and maintainance of bone calcium content during growth and development.

Animals↗

PubMed1998

Acute effects of prolactin on passive calcium absorption in the small intestine by in vivo perfusion technique.

The acute effect of intraperitoneally administered prolactin (0.2, 0.4, and 0.6 mg/kg body weight) on passive calcium transport in duodenum, proximal jejunum, and ileum of sexually mature female Wistar rats was investigated by using an in vivo perfusion technique. Test solution containing (in mM) NaCl, 100; KCl, 4.7; MgSO4, 1.2; CaCl2, 20; D-glucose, 11; sodium ferrocyanide (Na4Fe(CN)6), an index of net water transport, 20; and 0.7 microCi 45CaCl2 (1 Ci = 37 GBq) was perfused through the 10-cm intestinal loop for 60 min. Results showed that 0.4 mg prolactin/kg body weight significantly increased duodenal net Ca absorption (net Ca) from 23.81 +/- 1.84 to 30.56 +/- 1.57 mmol/g dry weight (p < 0.05) by stimulating the lumen to plasma calcium flux (CaL-P). The jejunum responded to 0.2, 0.4, and 0.6 mg prolactin/kg body weight by reversing from net Ca absorption of 18.60 +/- 1.70 mmol/g dry weight to net secretion of -3.30 +/- 1.56, -10.39 +/- 2.21, and -11.79 +/- 2.04 mmol/g dry weight (p < 0.01), respectively, as a result of a dose-dependent increase in plasma to lumen calcium flux (CaP-L). Calcium fluxes in the ileum on the other hand did not respond to prolactin. There was a close correlation between net water flux and net calcium flux in all three intestinal segments under basal condition regardless of the luminal sodium concentration. However, this correlation was lost after prolactin administration, which while having no effect on net water flux, altered the duodenal and jejunal calcium fluxes. By varying the luminal concentration of sodium, it was found that the stimulatory effect of 0.4 mg prolactin/kg body weight on the duodenal CaL-P was reduced when compared with control, i.e., 17.84 +/- 0.91 vs. 26.64 +/- 1.05 mmol/g dry weight at a sodium concentration of 180 mM, and 14.48 +/- 0.99 vs. 20.12 +/- 1.34 mmol/g dry weight at a sodium concentration of 140 mM. At a sodium concentration of 80 mM, the prolactin effect was absent. Since duodenal Na(+)-K+ ATPase activity was increased by prolactin from 3.77 +/- 0.16 to 4.95 +/- 0.30 mumol Pi.mg-1 protein.h-1 (p < 0.05), sodium dependency of the prolactin-enhanced lumen to plasma calcium flux may be related to both sodium-induced water flow and calcium-sodium exchange across the basolateral membrane. Thus, it was postulated that under basal condition, net calcium transport in the small intestine occurred with the sodium-induced water transport along the paracellular pathway. However, after prolactin administration, this association was lost. Prolactin-enhanced lumen to plasma calcium flux in the duodenum was sodium dependent and involved the Na(+)-K+ ATPase activity. In the proximal jejunum, prolactin stimulated plasma to lumen calcium flux, but the mechanism was not known.

Absorption↗

PubMed1998

The study of a physiological significance of prolactin in the regulation of calcium metabolism during pregnancy and lactation in rats.

Since a pharmacological dose of prolactin has previously been reported to enhance calcium absorption and bone calcium turnover, the role of endogenous prolactin in the regulation of calcium metabolism was investigated in the balance studies of Wistar rats between days 17 and 20 of first (P1) and fourth (P4) pregnancy and between days 12 and 15 of lactation (L). Each group was divided into 3 subgroups: one subgroup was given 0.9% NaCl (control); one was given 0.3 mg bromocriptine/100 g body weight ip twice daily for 3 days (to suppress prolactin secretion); and one was given bromocriptine and 0.25 mg prolactin/100 g body weight sc daily for 3 days. All three groups received 1 mL/100 g body weight of 1.25 mM calcium gluconate containing 2 mCi (1 Ci = 37 GBq) 45Ca daily for 3 days. Compared with the two pregnant controls, the L group had higher food consumption and higher fecal calcium excretion and lower urinary calcium excretion (% intake). Bromocriptine administration increased total calcium excretion from 59% intake to 84 and 66% intake in P1 and P4, respectively, suggesting that endogenous prolactin decreased total calcium excretion. On the other hand, exogenous prolactin had no effect on the calcium balance of P1 but increased the total calcium excretion in P4 from 57 to 66% intake. In contrast, the calcium balance of lactating rats was not altered by suppression of endogenous prolactin secretion or exogenous prolactin. Considering bone 45Ca content as representing bone Ca turnover, a lower value of bone 45Ca content indicated an accelerated bone Ca turnover. It was found that bromocriptine had no effect in P1 but decreased bone Ca turnover rate in the P4 and L groups, indicating an accelerating effect of endogenous prolactin on bone Ca turnover in the P4 and L groups. Exogenous prolactin, on the other hand, decreased bone Ca turnover rate in every group. Muscle Ca turnover was affected by bromocriptine and exogenous prolactin in the same manner as bone 45Ca contents. Interestingly, the biphasic action of prolactin was demonstrated in both calcium absorption and bone calcium turnover. It could be concluded that during pregnancy and lactation, endogenous prolactin increases food consumption, fractional calcium absorption, and bone calcium turnover, apparently to increase calcium availability for fetal development and milk calcium secretion.

Analysis of Variance↗

PubMed1997

Environment and the ageing lung.

A brief review of changes in the morphology, physiology and defence mechanism in the ageing lung is presented. During the ageing process, the lung is also affected by environmental insults, which can be exogenous or endogenous. Exogenous factors include infection, climate, air pollution and mechanical injuries, whereas endogenous environments are certain system diseases (e.g. diabetes mellitus and thromboembolism) as well as infectious diseases (e.g. tuberculosis).

Age Factors↗

PubMed1997

Acute effect of prolactin on bone 45Ca accumulation in rats.

In an attempt to evaluate the acute effect of PRL on bone turnover, experiments were performed in sexually mature female Wistar rats which were given an intraperitoneal (i.p.) administration of 1.25 mM CaCl2 solution containing 6 microCi 45Ca. Dose response study showed a two fold higher rate of 45Ca uptake in 30 min by control trabecular bones (sternum and vertebrae 5-6) compared with control compact bones (femur and tibia). Femur exhibited a dose dependent increase in 45Ca uptake in response to pharmacological doses of 0.01 and 0.02 mg PRL/100 g body weight but was less responsive to 0.04 mg PRL/100 g body weight. Tibia only responded with increased 45Ca uptake to 0.02 and 0.04 mg PRL/100 g body weight while trabecular bones were unresponsive. By varying the intervals between administration of 45Ca (0 min) and PRL (0, 30 or 60 min) and bone harvesting (30, 60 or 90 min), it was found that 0.01 mg PRL/100 g body weight had a biphasic action on 45Ca movement. It initially enhanced 45Ca influx into femur by 30 min followed by an accelerated 45Ca efflux from femur back to the circulation. It could be concluded that PRL acutely stimulated calcium turnover in compact bone.

Animals↗

PubMed1995

Acute and long-term effects of gastrin on muscle and bone calcium uptake in rats.

It has previously been proposed that the hypocalcemic action of gastrin was mediated by a gastric peptide gastrocalcin which enhanced bone uptake of calcium (Ca). The present study, thus, aimed to reconfirm the effect of gastrin on muscle and bone Ca uptake and to evaluate a possible direct effect of gastrin on tissue Ca uptake. First, we showed that human and rat gastrin (100 microgram /100 g body weight (bw), s.c.) acutely increased uptake of intragastrically administered 45 Ca by the tibia and femur. Interestingly, human gastrin was more effective and also enhanced 45 Ca uptake by the gastrocnemius muscle. In order to find out whether gastrin could act directly on bone, 10 microgram of rat gastrin /100 g bw and 45 Ca were injected into the right femoral artery supplying the right leg while the left leg received normal saline and an equal amount of 45 Ca. At 30 min, the right gastrocnemius muscle and femur were found to contain 168% and 162%, respectively, more 45 Ca than the left leg. In contrast, daily administration of 25 microgram of rat gastrins /100 g bw, s.c., for 2 weeks had no effect on muscle or bone total Ca content while the content of 45 Ca given on days 12 and 13 was lower in the tibia and femur of gastrin-treated rats. It could be concluded that gastrin transiently enhanced Ca uptake by muscle and bone. However, two-week treatment with gastrin appeared to accelerate the bone turnover rate i.e., enhanced uptake and release of calcium, so that there were not no net changes in bone total Ca content at the end of the experimental period.

Animals↗

PubMed1993

Acute effect and mechanism of action of prolactin on the in situ passive calcium absorption in rat.

Acute effect of prolactin (PRL) given intraperitoneally 1 h before on calcium fluxes was studied in 6 in situ intestinal segments from weaned, sexually mature and aged rats. In mature rats, PRL increased net passive calcium absorption in jejunum and cecum by 64% and 38%, respectively, by enhancing lumen-to-plasma calcium flux (CaL-P) in the jejunum and by reducing plasma-to-lumen flux (CaP-L) in the cecum. Since PRL-enhanced both CaL-P and CaP-L in the ileum, net calcium absorption did not change. In weaned rats, PRL significantly increased CaL-P in the jejunum but not in the ileum. However, the increase in net absorption was not significant. In contrast, effect of PRL was not seen in aged rats. By demonstrating an absence of PRL action on jejunal calcium fluxes when sodium-free test solution was used, we reconfirmed the sodium-dependent PRL action on passive calcium absorption. The PRL-induced parallel increase in the lumen-to-plasma transport of 45Ca and [3H]mannitol indicated that PRL action was to increase the paracellular transport of calcium.

Animals↗

PubMed1991

Further studies on acute effect of prolactin on intestinal calcium absorption in rat.

The present investigation aimed to (1) reconfirm the acute effect of prolactin on intestinal calcium absorption in the rat, (2) evaluate the influence of age on prolactin action, and (3) further investigate the mechanisms of prolactin action on calcium absorption. The intestinal calcium absorption in mature rats was evaluated by measuring the plasma 45Ca content at intervals during a 1-h period following intragastric administration of a 45Ca-containing test solution and by measuring tibial 45Ca content in weaned rats. By using weaned (50-70 g), sexually mature (180-200g) or aged (greater than 250 g) female Wistar rats, we demonstrated that calcium absorption was inversely related to age. Prolactin at a dose of 0.02 mg/100 g body weight, administered intraperitoneally 1 h before Ca administration, significantly enhanced calcium absorption in sexually mature and weaned rats but not in aged rats. At a luminal calcium concentration of 5 mM, prolactin had no effect when the luminal solution was either CaCl2 alone or an Na-free electrolyte solution. On the other hand, prolactin significantly increased the plasma 45Ca content by 57, 42 and 28% at 5, 15 and 30 min respectively, when the electrolyte solution contained sodium. In contrast, in the presence of 0.5 mM calcium, the enhancing effect of prolactin on calcium absorption was not dependent on the presence of sodium. Compared with the saline control, the plasma 45Ca content in prolactin treated animals was significantly elevated by 63% at 5 min when the test solution was a sodium-free electrolyte solution.

Aging↗

PubMed1990

Acute effect of prolactin on the intestinal calcium absorption in normal, pregnant and lactating rats.

Acute effect of prolactin on intestinal calcium absorption was studied in Wistar rats. Prolactin when given subcutaneously 24 h, or intraperitoneally 1 h, before intragastric administration of 45Ca-containing CaCl2 solution markedly increased the plasma 45Ca content. Of interest was the enhancing effect of prolactin on calcium transport seen in 1 h which suggested that prolactin could act directly on the intestine. Physiological significance of prolactin was evaluated in pregnant and lactating rats. Pretreatment with bromocriptine, an inhibitor of prolactin release, had no effect in rats on day 20 of pregnancy but significantly reduced calcium absorption in lactating rats. This reduced calcium absorption was only partially restored by prolactin treatment. The present investigation thus showed that prolactin, besides stimulating 1,25(OH2)D3 production, may also enhance calcium absorption directly. This effect was absent in pregnant rats but was of physiological significance in lactating rats.

Animals↗

PubMed1989

Different effects of bile and sodium taurocholate on mucosal calcium accumulation and calcium absorption in rats.

To demonstrate different effects of bile and Na taurocholate on calcium absorption, in vivo studies and in situ intestinal loop experiments were performed in intact rats. Only bile (collected from donor rats), but not 15 mM Na taurocholate, significantly increased the jejunal mucosa calcium and 45Ca contents after an intragastric administration of test solution containing 7.5 mM CaCl2 + 45Ca. However, plasma radioactivity which represented lumen to plasma calcium transport was increased by Na taurocholate but not bile, suggesting that both agents enhanced calcium transport across the brush border membrane but in the presence of bile some calcium remained in the mucosal cells. Results from the in situ studies supported the above findings. It was shown that bile and Na taurocholate enhanced the calcium transport from the lumen. However, net absorption was unchanged due to concurrent increase in the efflux of calcium.

Animals↗

PubMed1988

Biliary calcium and bile acid secretion in intact and TPTX rats with varying plasma calcium concentration.

Investigations of the effects of plasma calcium concentration on the relationship between biliary secretion of bile acid and calcium were performed in normocalcemic, calcium gluconate-induced hypercalcemic, thyroparathyroidectomy-induced hypocalcemic (TPTX) rats, and TPTX rats that received calcium gluconate to maintain normocalcemia. Studies were done at normal bile flow and at sodium taurocholate-stimulated bile flow. The results showed that biliary calcium secretion, which could occur in the absence of parathyroid hormone and calcitonin, was dependent mainly on plasma calcium concentration and was only partly influenced by bile acid secretion. Concerning the route of biliary calcium secretion, 80% was by the transcellular pathway and 20% was by the paracellular pathway. During theophylline-stimulated bile-acid-independent bile flow, the increase in bile-acid-independent calcium was found to be secreted by both pathways.

Animals↗

PubMed1988

Hemorrhage with blood reinfusion and the relationship between gastroduodenal motility and bile reflux in rats.

The relationship between gastroduodenal motility and bile reflux was studied in normal rats and in rats subjected to hemorrhage and blood reinfusion. Bile secretion decreased from 5.3 +/- 0.4 to 4.1 +/- 0.5 microL/(min.100 g rat) (p less than 0.05) during the hypovolemic stress and recovered after blood reinfusion. Gastric bile salt content was low (0.1 +/- 0.03 mumol/(h.100 g rat] during control period and hemorrhage but increased to 0.7 +/- 0.12 mumol/(h.100 g rat) (p less than 0.001) during the 3 h following blood replacement. Marked gastric and duodenal retention of polyethylene glycol was observed immediately after hypovolemia with the former being evident even after 3 h following blood reinfusion, while duodenal emptying recovered rapidly after reinfusion. The frequency of gastric contraction remained unchanged during hemorrhage but decreased after 90 min following blood replacement, whereas the frequency of duodenal contraction abruptly decreased during hemorrhage and recovered after reinfusion. Both gastric and duodenal contractile pressure was significantly decreased during hemorrhage. After reinfusion, the former remained suppressed while the latter was fully recovered within 1 h. Thus, a significant duodenogastric bile reflux observed after reinfusion was due to a higher duodenal contractile pressure, and the uncoordinated gastroduodenal motility with the duodenal motility fully recovered soon after reinfusion while that of the stomach remained suppressed.

Animals↗

PubMed1987

Mechanism of hypocalcemia induced by intraperitoneal, intragastric, and intravenous administration of ethanol to the rat.

Acute hypocalcemic effects of intraperitoneal administration of 3 and 5 g ethanol/kg body weight; intragastric administration of 3, 5, and 7 g ethanol/kg body weight; and intravenous administration of 2.5 a ethanol/kg body weight were investigated in 20 h fasted female Wistar rats. Dose-dependent hypocalcemia was similarly induced by intraperitoneal and intragastric routes of administration. Net calcium efflux from plasma, as indicated by the plasma 45Ca activity, was unaffected by 3 g ethanol/kg body weight but was delayed at higher doses of ethanol. Intragastric, but not intraperitoneal, administration of ethanol increased the gastrointestinal luminal calcium content partly by enhancing calcium secretion. Significantly increased tissue 45Ca content 30 min after ethanol administration was evident in the duodenum (31%), jejunum (27%), and colon (33%) in the intragastric ethanol-treated group and in the duodenum (40%), jejunum (38%), ileum (45%), colon (39%), and liver (25%) in the intraperitoneal ethanol-treated group. Thus, the hypocalcemia induced by both intraperitoneal and intragastric administration of ethanol could be partly accounted for by the suppression of calcium efflux from some soft tissues. In contrast, intravenous administration of ethanol was found to enhance the calcium efflux from plasma without affecting the net 45Ca content in the soft tissues. The mechanism(s) by which ethanol affects calcium transport has yet to be elucidated.

Animals↗

PubMed1987

The in vivo effect of ethanol on gastrointestinal motility and gastrointestinal handling of calcium in rats.

The acute effects of an intragastric administration of ethanol (2 g/kg body weight) (given as 13.3% w/v solution) on the in vivo gastrointestinal motility and gastrointestinal absorption and secretion of calcium were investigated in 20-h fasted rats. Gastric ethanol concentration remained high for 90 min while the concentration in the duodenum peaked at 30 min before declining to a range slightly higher than that in the mid- and distal intestine. Plasma ethanol peaked at 60 min. From the polyethylene glycol (PEG) distribution, ethanol was found to delay gastric emptying, and at 60 min, 40% of PEG was still retained in the stomach of the ethanol-treated group while gastric emptying had been completed in the controls. However, ethanol placed directly into the duodenum was found to enhance intestinal motility. Under control conditions, exogenous calcium was completely absorbed by the time it reached the mid-small intestine (J3) and calcium found in more distal segments was of endogenous origin. Ethanol suppressed calcium absorption while markedly stimulating calcium secretion in the stomach and the distal small intestine, resulting in a net 32% increase in the total gastrointestinal calcium content. This effect on the distal small intestine was from ethanol that had reached this area from the circulation, and not from ethanol transit along the gastrointestinal tract.

Animals↗

PubMed1986

Hypercalcemic effect of insulin in thyroparathyroidectomized alloxan-treated rats.

The acute effect of a hypoglycaemic dose of 0.5 U/100 g BW insulin administered intramuscularly on calcium metabolism was investigated in fasted alloxan-treated rats. It was found that the hypercalcaemic effect of insulin was evident only in thyroparathyroidectomized (TPTX) and not in parathyroidectomized (PTX) rats. A subcutaneous administration of 180 MRC mU/100 g BW calcitonin abolished the calcium raising effect of insulin in TPTX rats suggesting a protective role of calcitonin against insulin action in intact rats. In an attempt to elucidate the mechanism of the calcium raising effect of insulin 45Ca administered intravenously was used to indicate the movement of calcium from the plasma pool. Insulin administration delayed the plasma 45Ca disappearance rate but had no effect on bone 45Ca uptake within 120 min. In contrast, insulin administration resulted in a 31% reduction of urinary 45Ca excretion while the urine volume remained unchanged. However, the insulin-induced reduction of urinary calcium excretion could not totally account for the calcium raising effect of insulin in TPTX animals.

Animals↗

PubMed1984

Depression of estrogen-induced uterine peroxidase in alloxan-diabetic rats.

The influence of alloxan diabetes on reproductive function and the estradiol-stimulated increase in uterine peroxidase was investigated. Alloxan monohydrate in a dose of 75 mg/kg body weight effectively produced permanent diabetes. In adult rats, 20 days of diabetes resulted in cessation of the estrous cycle and a significant reduction in the gain of body weight, the weights of anterior pituitary gland, ovary, uterus, the level of serum progesterone and the activity of the estradiol-stimulated uterine peroxidase (P less than 0.05). After 10 days of insulin treatment, the ovarian weight, the estrous cycle and the level of ovarian hormones were restored to normal whereas the uterine weight and the estradiol-stimulated uterine peroxidase activity were only partially recovered. Persistent depression of the uterine response in the insulin-treated diabetic rats to both endogenous and exogenous ovarian hormone stimulation suggests that the uterus was directly affected by diabetes. The direct effect of diabetes upon the uterus was further demonstrated in the ovariectomized immature rat in which diabetes depressed the stimulatory action of estradiol on both uterine weight and uterine peroxidase activity.

Animals↗