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Biomedical subjects

T Bjøro

Publications and source records attributed to T Bjøro.

At least 19 recordsLinked to original sources
PubMed2006

Treatment-related premature ovarian failure as a long-term complication after Hodgkin's lymphoma.

BACKGROUND: One of the medical sequelae that chemo- and radiotherapy may cause is premature ovarian failure (POF). The scope of this study was to investigate the risk of developing POF as a long-term complication in young women treated for Hodgkin's lymphoma. PATIENTS AND METHODS: The 99 women included in the study were treated between 1975 and 1992 at the Norwegian Radium Hospital. All patients received radiotherapy and 67 of the women also received chemotherapy. RESULTS: POF was found in 37.4% of the patients. The risk of developing POF was significantly higher if the patient received chemotherapy in addition to radiotherapy. Furthermore, the risk increased if chemotherapy included alkylating agents. Long-term follow-up revealed that women who at the time of treatment were under 30 years of age developed POF later, but with the same cumulative risk as women above 30 years of age. CONCLUSIONS: The risk of developing POF after radio- and chemotherapy is higher than earlier estimates suggest. After an observation time of 15 years the cumulative risk is 38% independent of age at the time of treatment. Age below 30 years at the time of treatment delays the development of POF, but does not decrease the life-time risk.

Adolescent↗
PubMed2003

Recovery of skeletal muscle contractility and hormonal responses to strength exercise after two weeks of high-volume strength training.

Exercise induced neuromuscular fatigue, recovery and hormonal responses were studied before (R1) and after (R2) 2 weeks of heavy strength training. Seventeen weight-trained male students were recruited into a heavy training group (HT, n = 10) and a control group (n = 7). During heavy training HT exercised leg extensors every day while control group exercised twice a week. Test workouts (R1 and R2) were used to induce neuromuscular fatigue and hormonal responses. Acute fatigue after the test workouts was reduced after heavy training in the HT group (P < 0.05) but not in the control group. Twenty-two hrs after the test workouts recovery from fatigue was not complete before heavy training, but recovery was complete after heavy training in both groups. The relative change in exercise induced cortisol and GH response, from before to after heavy training, was significantly different between groups, but for both hormones alterations in the control groups response was responsible for the between groups difference. IGF-1 concentration was reduced 22 h after the test workout performed after heavy training in the HT group (P < 0.05). In conclusion, two weeks of high volume strength training attenuated neuromuscular fatigue after a test workout with only minor changes in exercised induced hormone response.

Adult↗
PubMed2003

Secondary osteoporosis in liver transplant recipients: a longitudinal study in patients with and without cholestatic liver disease.

BACKGROUND: Metabolic bone disease is one of the major long-term complications in liver transplant recipients, but it remains unclear which patients are at highest risk for developing severe bone disease following transplantation. METHODS: A total of 46 consecutive, adult patients with chronic liver disease accepted for a liver transplantation waiting list were prospectively included in the study. The patients were classified into two groups: group A--chronic cholestatic liver disease (n = 28), and group B--chronic non-cholestatic liver disease (n = 18). Bone mineral density (BMD) was measured at acceptance for the waiting list and at 3, 12 and 36 months following transplantation. Markers of bone turnover (serum-bone specific alkaline phosphatases (bALP), s-osteocalcin, s-1-collagen-C-terminal telopeptide (1-CTP) and urine N-terminal telopeptides u-Ntx) were measured at acceptance and at 3, 6, 12, 24 and 36 months following transplantation. BMD and markers of bone turnover were compared with similar values in a matched control group of 42 healthy individuals. RESULTS: BMD decreased significantly during the early post-transplantation period (median bone loss femoral neck (FN) 3 months post-transplant 8.5%). BMD levels declined slightly from 3 to 12 months following transplantation and increased thereafter. The relative bone loss was greatest among group B patients (relative bone loss FN 3 months post-transplant: group A, 8% versus group B, 13%; P = 0.04). At 36 months, 8/17 group A and 2/9 group B patients had BMD levels that exceeded the pretransplant levels (P = 0.12). The early bone loss was positively correlated with an increase in resorption markers (s-1-CTP and u-Ntx). Group B had higher levels of both s-1-CTP and u-Ntx at 3 and 6 months post-transplant than group A patients (P = 0.03). Bone formation markers increased slowly from 6 months post-transplant and onwards. Relative bone loss was positively correlated to total glucocorticoid dose during the first 3 months post-transplant. There were no differences in BMD between patients receiving tacrolimus versus those receiving cyclosporin A. CONCLUSION: Bone loss following liver transplantation is considerable in patients with both cholestatic and non-cholestatic liver disease, the first group has the poorest starting-point while the latter group has the greatest bone loss following transplantation. Bone loss is closely correlated with biochemical markers of bone resorption and total dose of glucocorticoids given post-transplant.

Adult↗
PubMed2002

Thyroid dysfunction during treatment of chronic hepatitis C with interferon alpha: no association with either interferon dosage or efficacy of therapy.

OBJECTIVES: Treatment of chronic hepatitis C with interferon-alpha (IFN-alpha) may induce thyroid disorders. We evaluated whether this risk is related to the dosage of IFN-alpha or the virological treatment response. Other possible risk factors as well as the evolution of the thyroid abnormalities were also studied. METHODS: In this prospective trial (n=254), thyroid-stimulating hormone (TSH), free thyroxin (fT4) and thyroid peroxidase autoantibodies were measured before, during and after treatment for hepatitis C virus (HCV). The patients were randomized to either induction therapy [IFN-alpha 6 million units (MIU) daily for 4 weeks and 3 MIU 3/7 days for 22 weeks] or conventional therapy [IFN-alpha 3 MIU 3/7 days for 26 weeks]. In addition, all patients received ribavirin (1000 or 1200 mg) daily. Sustained virological response was defined as loss of detectable HCV RNA at 6 months follow-up. Thyroid dysfunction was defined as TSH level below or above the normal range (0.2-4.5 MIU L-1). RESULTS: Biochemical thyroid dysfunction developed in 30 (11.8%) of 254 patients. Hypothyroidism (TSH > 4.5 MIU L-1) was seen in 20 and hyperthyroidism (TSH < 0.2 MIU L-1) in 10 patients. Nine of the 30 patients developed symptomatic thyroid disease and HCV treatment was discontinued because of thyroid dysfunction in three of these patients. Thyroid dysfunction occurred in 15 (11.7%) of 128 patients who received high-dose IFN-alpha induction therapy as compared with 15 (11.9%) of 126 patients who received conventional IFN-alpha therapy (P=0.96). Amongst 231 patients who completed all 6 months of HCV treatment, a sustained virological response was obtained in 19 (66%) of 29 with thyroid dysfunction and 109 (54%) of 202 without (P=0.24). By multivariate analysis female gender and Asian origin were independent predictors of developing biochemical thyroid dysfunction (P < 0.01). CONCLUSION: Thyroid dysfunction occurred in 11.8% of patients treated for chronic hepatitis C with IFN-alpha and ribavirin. Neither the IFN-alpha dosage nor the virological response to treatment were related to the incidence of thyroid dysfunction.

Adult↗
PubMed2001

[Psychiatric and cognitive aspects of hypothyroidism].

BACKGROUND: Diffuse and initial changes of behaviour, mood and cognition in hypothyroidism represent diagnostic and therapeutic challenges. MATERIAL AND METHODS: We present four cases and discuss relevant literature. Patients were followed from time of diagnosis through the first 6-12 months of thyroxine treatment. Symptoms were identified using interviews, questionnaires and tests. RESULTS: The patients had reduced quality of life, depression, anxiety and impaired short time memory. All symptoms improved with thyroxine treatment, although patients did not necessarily reach premorbid functioning in 6-12 months. In the literature, depression in hypothyroidism is hypothesised to be at least partly caused by relative hypothyroidism in the central nervous system, and local brain triiodothyronine deficiency may be a possible explanation for affective and cognitive symptoms in subclinical hypothyroidism. INTERPRETATION: Physicians should actively address psychiatric and cognitive aspects of hypothyroidism and in addition to thyroxine offer supportive treatment, especially to those depressed.

Adult↗
PubMed2001

Low headache prevalence amongst women with high TSH values.

The aim of this large cross-sectional population-based study was to examine a possible positive or negative association between thyroid dysfunction and headache. Between 1995 and 1997, all 92 566 adults in Nord-Trøndelag County in Norway were invited to participate in a health survey. A total of 51 383 (56%) responded to a headache questionnaire, whereof thyroid-stimulating hormone (TSH) was measured in 28 058 individuals. These included 15 465 women and 8019 men above 40 years of age, 1767 randomly selected individuals between 20 and 40 years of age, and 2807 (97%) with thyroid dysfunction. Associations between thyroid dysfunction and headache were assessed in multivariate analyses, estimating prevalence odds ratios (OR) with 95% confidence intervals (CIs). High TSH values were associated with low prevalence of headache. This was most evident amongst women with no history of thyroid dysfunction. Amongst these, headache was less probable (OR=0.5, 95% CI 0.3-0.7) if TSH > or = 10 mU/l than in women with normal TSH (0.2-4 mU/l). In all age groups between 40 and 80 years, TSH was lower amongst headache sufferers, especially migraineurs, than in those without headache complaints.

Adult↗
PubMed2001

Distinct guanine nucleotide binding protein alpha-subunit receptor coupling in GH cell lines: effects of bromocriptine and hormones on effector enzyme modulation.

The purpose of the present study was to elucidate how the dopamine agonist bromocriptine affected receptor-effector systems in GH cells by measuring adenylate cyclase (AC) and phospholipase C (PL-C) modulation in cell membrane preparations. To perturb the interaction between the receptor and G-protein, polyclonal antibodies reacting with the predicted C-terminal amino acid sequence of G-protein alpha-subunits were used. The effect of bromocriptine on secretagogue elicited prolactin (PRL) secretion from whole cells was also monitored. Bromocriptine inhibited the basal secretion of PRL in a dose dependent manner, and completely abolished both the thyroliberin (TRH) and the vasoactive intestinal peptide (VIP) stimulated PRL secretion in GH(3) cells. Maximal inhibitory effect on PRL egress elicited by both hormones was obtained at 10-50 microM of bromocriptine. Messenger RNAs for both the short and long form of the D(2) receptor (D(2)R) were demonstrated in all three GH cell lines using the RT-PCR technique, advocating that D(2)Rs are coupled to distinct G-proteins and, thus, probably being responsible for the observed effects of bromocriptine in these cell lines. Basal AC activity, as measured in membrane preparations of GH(3) cells, remained unaffected by bromocriptine treatment (10 microM), while TRH and VIP stimulated AC activities (175% and 350% of control values, respectively) were partially inhibited (by some 50%). This inhibitory effect of bromocriptine was completely and specifically abolished in the presence of an antiserum against G(i2)alpha. Basal PL-C activity was also unaffected by bromocriptine, while TRH stimulated PL-C activity (350% of control value) was inhibited by bromocriptine (10 microM) by approximately 50%. Immunoblocking of G(q/11)alpha, however, reduced the stimulatory effect of TRH on PL-C activation by some 65%, while an antiserum against G(o)alpha partly counteracted the inhibitory effect of bromocriptine (10 microM) on TRH stimulated PL-C activity. Thus, TRH dependent AC stimulation was counteracted by bromocriptine via G(i2). TRH activation of PL-C occurs via G(q/11), while inhibition by bromocriptine appears to involve G(o). These mechanisms probably account for the major part of the actions of bromocriptine, however, other not yet recognised intermediates may be involved.

Adenylyl Cyclases↗
PubMed2000

Hormonal responses to high- and moderate-intensity strength exercise.

The hormonal responses of nine male, strength athletes to strength exercise were examined. The athletes performed one moderate- and one high-intensity strength exercise workout. In the high-intensity workout, the load was 100% of each subject's three-repetition maximum (3-RM) for squats and front squats, and 100% of each subject's six-repetition maximum (6-RM) for leg extensions. In the moderate-intensity workout, the load was 70% of the high-intensity protocol. Rest periods between sets were 4-6 min for both workouts. Blood samples were taken before, 30 min into, and every 15 min for the 1st h after exercise, and then 3, 7, 11, 22 and 33 h after exercise, thus allowing examination of both the acute and prolonged hormonal responses. Blood samples were analyzed for testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH), cortisol, adrenocorticotrophic hormone (ACTH), growth hormone (GH), insulin-like growth factor (IGF-1), insulin, sex hormone binding globulin, creatine kinase, total protein, glucose and lactate. The acute responses of testosterone and cortisol were greater during the high-intensity protocol as compared to the moderate-intensity protocol. The cortisol response was associated with an increase in ACTH concentration. LH and FSH showed no response to either protocol. Acute GH responses were not different between protocols. There were great inter-individual differences in acute GH responses to both protocols. There were no significant differences between protocols with regard to prolonged responses for any hormone. In both trials, IGF-1 concentrations were significantly lower at 0800 hours the morning after exercise as compared to concentrations found at 0800 hours the morning before exercise. The mechanisms responsible for reducing IGF-1 concentration in these trials are unclear, and it is not known if this reduction observed 22 hours after exercise is of physiological significance.

Adrenocorticotropic Hormone↗
PubMed2000

Perfusion system for studying peptide secretion from endocrine cells with high time resolution.

To study the secretion from endocrine cells in culture, we have developed a cell column perfusion system with a time resolution of 4 s. The core of the system is a perfusion chamber with a cell-supporting matrix of monosized polystyrene beads. The particles are solid and can withstand a high pressure gradient without deformation. The minimum amount of cell material required to obtain detectable levels of secretory products is a function of the assay sensitivity, perfusion flow, fraction volume and time resolution. The volume of the perfusion chamber is therefore adjustable to satisfy varying demands of minimum cell number. The general flow characteristics of the system were characterized using radiolabeled substances of various molecular sizes. Using the system in secretory studies of rat pituitary tumor (GH4C1) cells, we have identified differences in secretion profiles that may be related to the kinetics of the different transmembrane and intracellular mechanisms involved.

Animals↗
PubMed1997

Serum N-terminal pro-atrial natriuretic factor 1-98 before and during thyroxine replacement therapy in severe hypothyroidism.

Decreased plasma concentrations of atrial natriuretic factor (ANF) and of its N-terminal prohormones have been demonstrated in severely hypothyroid patients compared with control subjects, and shown to normalize with thyroxine (T4) replacement therapy. Whether this depends on thyroid hormone deficiency exclusively or is secondary to hemodynamic changes that result from it remains a matter of debate. In a recent investigation dose-related increases in both ANF and N-terminal prohormones of ANF by T4 replacement therapy in incremental doses increased at 4-week intervals were demonstrated. It was suggested that thyroid hormones may enhance synthesis rather than release of atrial peptide hormones. The aim of the present study was to confirm this assumption in hypothyroid patients with normal cardiac performance. Serum N-terminal amino acids 1-98 (ie, pro-ANF 1-98) of pro-ANF was determined in 11 severely hypothyroid patients without pericardial effusion and with normal cardiac left ventricular function. Mean pro-ANF 1-98 concentration before T4 replacement therapy remained unchanged after 10 days on T4 (p = .12). After 2 months of therapy, mean pro-ANF 1-98 was significantly increased compared with pretreatment values (p < .003). A significant correlation to the increase in free T4 (r = 0.48, p < .01) but not to the decrease in thyrotropin (TSH) (r = -0.32, p = .09) was found. The present results indicate that thyroid hormones directly increase pro-ANF 1-98 independently of cardiac hemodynamics in the hypothyroid state.

Adult↗
PubMed1997

Both growth hormone and exogenous glutamine increase gastrointestinal glutamine uptake in trauma.

OBJECTIVE: The authors studied the effect of exogenous glutamine (GLN), with and without growth hormone (GH), pretreatment, on gastrointestinal, hepatic, femoral, and renal GLN fluxes. SUMMARY BACKGROUND DATA: Growth hormone treatment increases gastrointestinal uptake of GLN despite a reduced skeletal muscle and whole body release. METHODS: Piglets were randomized to a GH + GLN group (n = 8), a GLN group (n = 8), a GH group (n = 8), and a control group (CON; n = 8). Genotropin (Pharmacia, Stockholm, Sweden; 24 international units; correspondingly saline in the GLN and the CON group) was given daily 3 days before and at the onset of trauma (surgery). Organ fluxes and whole body release of GLN were determined 1 and 5 hours after surgery. An infusion of GLN 36 micrograms/kg per minute was started after the first measurement in the GH + GLN and the GLN groups. RESULTS: Both GH treatment and exogenous GLN increased gastrointestinal GLN uptake (p = 0.001 and p = 0.02, respectively). Growth hormone treatment reduced hepatic GLN uptake (p = 0.001). Hepatic GLN uptake was lower in the GH + GLN group versus the GH group (p = 0.02), but not in the GLN group versus the CON group (p = 0.98). Growth hormone treatment reduced femoral and whole-body GLN release (p = 0.0001 and p = 0.02, respectively). Renal GLN uptake was higher in the two GH-treated groups (p = 0.003). CONCLUSION: Both exogenous GLN and GH increased gastrointestinal GLN uptake, and the combination was additive. In contrast to exogenous GLN, GH reduced hepatic uptake and consequently facilitated the increased gastrointestinal GLN uptake that occurred despite reduced femoral and whole-body release.

Animals↗
PubMed1995

Frequency of hyperprolactinaemia due to large molecular weight prolactin (150-170 kD PRL).

Of 605 hyperprolactinaemic sera (prolactin > 1000 mU l-1 determined with PRL DELFIA, Wallac) in the routine diagnostic (PRL was measured in 10,737 sera) 26% had an increased amount of PRL with molecular weight (MW) = 150-170 kD (150-170 kD PRL or bigbig PRL). In a series of serum samples from 660 healthy subjects, only one female with hyperprolactinaemia due to increased 150-170 kD PRL was found. The 150-170 kD PRL constituted less than 1% of the total PRL found in 11 patients with prolactinoma (macroprolactinoma, PRL 8800-500,000 mU l-1). When determined with five different commercially available immunometric assays, the PRL values in the sera with large amounts of 150-170 kD were increased in all sera in four of five assays, although they varied widely. The clinical implications of hyperprolactinaemia due to increased 150-170 kD PRL are still uncertain.

Adult↗
PubMed1995

Metabolic effects of two regimens of growth hormone given before operation in piglets.

OBJECTIVE: To clarify the effects of growth hormone (GH) given three days before and at the start of a standard abdominal operation or at the start of the abdominal operation alone in piglets. DESIGN: Randomised experiment. SETTING: University hospital, Norway SUBJECTS: Twenty-four piglets. INTERVENTIONS: GH 24 IU was given intramuscularly for either three days before and on the morning of the operation or on the morning of a standard abdominal operation only (n = 8 in each group) A further 8 piglets acted as untreated controls. MAIN OUTCOME MEASURES: Diameter of fibres in the soleus and gastrocnemius muscles; urinary nitrogen excretion; and fat and carbohydrate oxidation measured by indirect calorimetry. RESULTS: Nitrogen excretion was reduced (in the three days group the mean (SEM) was 30.8 (4.2) mg/kg, corresponding figures from the one day group and the controls were 37.6 (5.8) and 55.4 (3.1) mg/kg, respectively, p = 0.004). Fat oxidation increased (for the whole period: p = 0.014) and carbohydrate oxidation decreased (p = 0.02) in the one day group only. The diameter of type I muscle fibres was increased in both muscles (soleus, three day group, mean (SEM) 37.5(1.4) microns compared with control, 30.4(0.6) microns, p = 0.001, and gastrocnemius, three day group 38.6(1.3) microns compared with control, 30.8(1.4) microns, p = 0.01). CONCLUSIONS: Three days treatment with GH enhanced nitrogen sparing and attenuated changes in fat and carbohydrate oxidation induced by one day treatment, but induced hypertrophy of type I muscle fibres.

Animals↗
PubMed1994

Calcitriol attenuates the basal and vasoactive intestinal peptide-stimulated cAMP production in prolactin-secreting rat pituitary (GH4C1) cells.

A clonal strain of prolactin-producing rat pituitary tumour cells (GH4C1 cells) was used to study the effect of calcitriol on cyclic adenosine monophosphate (cAMP) production. Calcitriol (10 nM) attenuated both the basal and vasoactive intestinal peptide (VIP)-stimulated cAMP production after 2 days' pretreatment of the cells. The effect was detectable at 1 nM and maximal at about 10 nM. Calcitriol was at least 100 times more potent than calcidiol and 24-hydroxycalcidiol. Calcitriol (10 nM, 4 days) did not affect the specific binding of 125I-VIP, but attenuated the guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS)-stimulated (100 microM) adenylyl cyclase activity by 25%. Calcitriol (10 nM, 4 days) also attenuated both the Mn2+ (1 mM) and the forskolin-stimulated (10 microM) adenylyl cyclase activity by 43 and 41%, respectively. In conclusion, these data suggest that calcitriol attenuates the basal and VIP-stimulated cAMP production by inhibiting the catalytic subunit of the adenylyl cyclase as well as the amount of the G protein Gs alpha.

Animals↗
PubMed1994

Vitamin D receptor binding and biological effects of cholecalciferol analogues in rat thyroid cells.

The cholecalciferol analogues 1(S),3(R)-dihydroxy-20(R)-[3'(S)-cyclopropyl-3'-hydroxyprop-1'(E)- enyl]-9,10-secopregna-5(Z),7(E),10(19)-triene (calcipotriol, MC 903), 1(S),3(R)-dihydroxy-20(R)-[3'-ethyl-3'-hydroxy- pentoxy]-9,10-secopregna-5(Z),7(E),10(19)-triene (KH 1060) and 1(S),3(R)-dihydroxy-20(R)-[5'-ethyl-5'-hydroxy-hepta- 1',3'(E)-diene-1'-yl]-9,10-secopregna-5(Z),7(E),10(19)-triene (EB 1089) have been modified in the side chain to increase their effects on cell differentiation and proliferation and to reduce the risk of inducing hypercalcemia. The effects of these analogues were tested on FRTL-5 cells, a strain of continuously growing and well-differentiated rat thyroid cells. FRTL-5 cells express a normal vitamin D receptor (VDR), and 1,25-(OH)2D3 potently attenuates the thyrotropin (TSH) stimulated production of the intracellular signalling molecule 3',5'-cyclic adenosine monophosphate (cAMP), iodide uptake and cell growth of these cells. These effects were also induced by the cholecalciferol analogues after 4 days of incubation. KH 1060 was the biologically most potent of the analogues and, compared to KH 1060, the IC50 values were 1.2-, 2.7- and 14-fold higher when 1,25-(OH)2D3, EB 1089 and MC 903, respectively, were used for the displacement of receptor bound [3H]1,25-(OH)2D3. As indicated by their VDR binding, 1,25-(OH)2D3 and EB 1089 were equipotent inhibitors of the TSH stimulated adenylyl cyclase activity, iodide uptake and FRTL-5 cell growth. The analogue MC 903 was the second most potent inhibitor of cell growth in spite of expressing the lowest affinity for the VDR and the weakest inhibition of TSH-stimulated adenylyl cyclase activity and iodide uptake. In conclusion, the biological effects of these cholecalciferol analogues in rat thyroid FRTL-5 cells seem to be mainly determined by their binding affinity for the VDR, although non-genomic effects can not be excluded.

Adenylyl Cyclases↗
PubMed1994

1,25-Dihydroxyvitamin D3 attenuates adenylyl cyclase activity in rat thyroid cells: reduction of thyrotropin receptor number and increase in guanine nucleotide-binding protein Gi-2 alpha.

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] is the most potent of the naturally occurring vitamin D metabolites. In rat thyroid FRTL-5 cells, 1,25-(OH)2D3 attenuated the increase in TSH-stimulated adenylyl cyclase activity obtained by removing TSH from the culture medium. When cells were incubated with 1,25-(OH)2D3 (10 nmol/liter; 4 days), the binding capacity for specific [125I]TSH binding decreased from 20.1 +/- 1.8 to 8.8 +/- 1.6 fmol/10(6) cells (mean +/- SEM; n = 4; P < 0.01) compared to that in control cells. The Kd did not change (mean +/- SEM, 0.46 +/- 0.09 vs. 0.25 +/- 0.07 nmol/liter; n = 4; P = NS). Western blotting revealed no change in the membrane content of the adenylyl cyclase (AC) stimulatory guanine nucleotide-binding protein (G-protein) alpha-subunit (Gs alpha) during 1,25-(OH)2D3 treatment. Similarly, levels of the AC inhibitory G-protein Gi-3 alpha- and G-protein beta-subunits were not altered by 1,25-(OH)2D3. However, Western blotting with antibodies recognizing both Gi-1 alpha and Gi-2 alpha was augmented 4-fold, presumably representing an increase in Gi-2 alpha only, as Gi-1 alpha messenger RNA (mRNA) was not detected in FRTL-5 cells. 1,25-(OH)2D3 (10 nmol/liter; 4 days) reduced cholera toxin (10 nmol/liter)-stimulated AC activity to 85% of the control value (P < 0.05), whereas forskolin (100 mumol/liter)-stimulated direct activation of AC was inhibited by 39%. The TSH receptor mRNA level correlated to the beta-actin mRNA was 2-fold higher in control cells compared to that in 1,25-(OH)2D3-treated cells 12 h after TSH removal. Only minor alterations in the Gs alpha mRNA/beta-actin mRNA and Gi-3 alpha mRNA/beta-actin mRNA ratios were observed during 1,25-(OH)2D3 treatment, whereas Gi-2 alpha mRNA increased 3-fold compared to that in control cells. No change in the resting intracellular Ca2+ concentration could be detected after 4 days of 1,25-(OH)2D3 treatment. Our studies show that 1,25-(OH)2D3 attenuates AC activity by reducing the TSH receptor number and increasing the level of the AC inhibitory G-protein Gi-2 alpha in FRTL-5 cells.

Actins↗
PubMed1993

Growth hormone treatment after abdominal surgery decreased carbohydrate oxidation and increased fat oxidation in patients with total parenteral nutrition.

Patients undergoing elective abdominal surgery were double-blindly randomized for treatment with growth hormone (GH) 24 IU (n = 9) or placebo (n = 10) the first 5 postoperative days while receiving total parenteral nutrition (nitrogen, 5.7 +/- .1 g/m2; energy, 1,018 +/- 12 kcal/m2, ie, 125% +/- .7% of basal metabolic rate [BMR]). Carbohydrate and fat metabolism were evaluated from indirect calorimetry, daily blood samples, and forearm substrate-flux studies. Hormone levels in plasma or blood were also determined. GH decreased carbohydrate oxidation, increased fat oxidation, and increased resting energy expenditure (REE). Free fatty acids (FFA), glycerol, and beta-hydroxybutyrate (beta-OH-B) levels increased in both arterial and venous plasma, and forearm release of FFA and glycerol increased. GH, insulin-like growth factor 1 (IGF-1), and glucagon levels in venous blood were also increased in GH-treated patients. Thus, GH induced mobilization and utilization of fat, and fat was preferred to glucose for energy requirements in patients after abdominal surgery with nutritional support.

Adult↗