Enhancement by hypophysectomy of insulin effect on extrahepatic galactose transfer

1961 ◽  
Vol 200 (6) ◽  
pp. 1311-1314 ◽  
Author(s):  
Norio Kokka ◽  
Leslie L. Bennett
Keyword(s):  
Blood Glucose Concentration ◽  
Equilibrium Concentration ◽  
Distribution Volume ◽  
Blood Levels ◽  
Volume Distribution ◽  
Insulin Effect ◽  
Hypophysectomized Rats ◽  
Prior Administration ◽  
Insulin Hypersensitivity ◽  
Normal Controls

Fasted, normal, and hypophysectomized rats were eviscerated and nephrectomized under light pentobarbital anesthesia. Glucose was infused intravenously at rates that maintained a nearly constant blood glucose concentration. Single injections of galactose were given that produced an equilibrium concentration at 60 min of 247 ± 30 mg%. The galactose level was not significantly different at 90 min. Thus insulin could be administered at 60 min and the 60–90 min blood galactose change used as an index of insulin action. The extrahepatic uptake of galactose in hypophysectomized rats was demonstrated to be hypersensitive to insulin by two criteria: a) significant decreases in blood galactose concentration of hypophysectomized rats were produced by 0.01 unit of insulin/kg, a dose that had no effect on normal rats; b) after 0.02 unit of insulin/kg, changes in blood levels of galactose were greater in hypophysectomized rats than in their normal controls. Hypophysectomy did not alter galactose distribution volume. In neither normal nor hypophysectomized rats did prior administration of growth hormone alter either volume distribution of galactose or insulin hypersensitivity.

INFLUENCE OF THIAZIDES ON THYROID PARAMETERS IN MAN

1978 ◽  
Vol 89 (4) ◽  
pp. 673-678 ◽  
Author(s):  
Karine Bech ◽  
Lis Skovsted ◽  
Kaj Siersbæk-Nielsen ◽  
Jens Mølholm Hansen
Keyword(s):  
Arterial Hypertension ◽  
Urinary Iodine ◽  
Iodine Intake ◽  
Term Treatment ◽  
Distribution Volume ◽  
Long Term Treatment ◽  
Thyroid Uptake ◽  
Iodine Metabolism ◽  
Normal Controls

ABSTRACT Iodine metabolism and thyroid hormones in blood were studied in 19 men and 11 women who had been treated with thiazides for arterial hypertension from 1 month to 15 years. The results were compared with the findings from age-matched normal controls. No differences were found regarding 24-h 131I-thyroid uptake, thyroid iodide clearance, renal iodide clearance, plasma inorganic iodide, absolute iodine uptake (AIU), serum thyroxine (T4 (D)), resin T3 test (T3U) and TSH after TRH. Twenty-four-hour urinary iodine was higher in the patients treated with diuretics which could be explained by increased iodine intake. The findings of increased serum triiodothyronine (T3 (RIA)) and reverse T3 (rT3) might be due to changes in distribution volume in the thiazide-treated patients. Long-term treatment with thiazides in man do not lead to iodine depletion.

scholarly journals Subcutaneous adipocytes from obese hyperinsulinemic women with polycystic ovary syndrome exhibit normal insulin sensitivity but reduced maximal insulin responsiveness

2005 ◽  
Vol 153 (6) ◽  
pp. 831-835 ◽  
Author(s):  
Erika Lystedt ◽  
Hanna Westergren ◽  
Jan Brynhildsen ◽  
Lotta Lindh-Åstrand ◽  
Johanna Gustavsson ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Subcutaneous Fat ◽  
Diabetic Control ◽  
Control Group ◽  
Blood Levels ◽  
Ovary Syndrome ◽  
Insulin Effect

Background: Polycystic ovary syndrome (PCOS) has a high prevalence in women and is often associated with insulin resistance and hence with aspects of the so-called metabolic syndrome. Methods: Ten women diagnosed with PCOS were consecutively included (aged 21–39 years, average 30.2 ± 1.9 years; body mass index 28.4–42.5 kg/m2, average 37.5 ± 1.7 kg/m2 (mean ± s.e.)). Adipocytes were isolated from the subcutaneous fat and, after overnight incubation to recover from insulin resistance due to the surgical cell isolation procedures, they were analyzed for insulin sensitivity. Results: The patients with PCOS exhibited marked clinical hyperinsulinemia with 3.6-fold higher blood levels of C-peptide than a healthy lean control group (1.7 ± 0.2 and 0.5 ± 0.02 nmol/l respectively, P < 0.0001). The patients with PCOS also exhibited 2.4-fold higher concentrations of serum triacylglycerol (2.1 ± 0.3 and 0.9 ± 0.06 mmol/l respectively, P < 0.0001), but only slightly elevated blood pressure (118 ± 12/76 ± 6 and 113 ± 7/72 ± 6 mmHg respectively, P = 0.055/0.046). However, insulin sensitivity for stimulation of glucose transport in the isolated adipocytes was indistinguishable from a non-PCOS, non-diabetic control group, while the maximal insulin effect on glucose uptake was significantly lower (2.2 ± 0.2- and 3.8 ± 0.8-fold respectively, P = 0.02). Conclusions: Subcutaneous adipocytes from patients with PCOS do not display reduced insulin sensitivity. The findings show that the insulin resistance of PCOS is qualitatively different from that of type 2 diabetes.

Hypothalamic neurohormonal agents and sexual maturation of immature female rats

1961 ◽  
Vol 201 (6) ◽  
pp. 1176-1180 ◽  
Author(s):  
Alan Corbin ◽  
B. A. Schottelius
Keyword(s):  
Reproductive Organ ◽  
Female Rats ◽  
Albino Rats ◽  
Immature Female ◽  
Organ Growth ◽  
Hypophysectomized Rats ◽  
Bilateral Destruction ◽  
The Brain ◽  
Normal Controls

The possible role of four recognized hypothalamic constituents in activation and maturation of the hypophysial-reproductive organ complex of immature female albino rats was investigated. Normal and hypophysectomized rats and rats with bilateral destruction of an area extending from the ventromedial nucleus to mammillary body were studied. Animals were injected either with 70 milliunits of antidiuretic hormone (ADH), 70 milluniits of oxytocin, 25 µg of serotonin, or 2 µg of epinephrine every 5th day, from age 20 through 45 days, via a cannula permanently implanted in the 3rd ventricle of the brain. No response to ADH was observed. Oxytocin accelerated vaginal canalization and caused premature reproductive organ growth in normal recipients. Whereas lesioned untreated controls remained sexually retarded, vaginal opening and reproductive organ growth equivalent to 50-day-old sham-operated controls were induced in lesioned animals by oxytocin administration. Serotonin prevented maturation in normal controls, but was ineffective in lesioned animals. Hypophysectomized rats were unresponsive to any agent injected. The results imply that oxytocin may directly activate the hypophysis of immature female rats. Serotonin, on the other hand, inhibits the hypophysial-gonadal axis of these animals, but its effects probably are relayed via the hypothalamus.

EFFECTS OF TRANSPLANTED PITUITARY GLANDS FROM NON-ARTERIOSCLEROTIC VIRGIN AND ARTERIOSCLEROTIC BREEDER DONORS TO HYPOPHYSECTOMIZED RATS

1968 ◽  
Vol 59 (2) ◽  
pp. 249-260 ◽  
Author(s):  
Bernard C. Wexler ◽  
Jack Saroff
Keyword(s):  
Female Rats ◽  
Degenerative Diseases ◽  
Male And Female ◽  
Histological Evidence ◽  
Serum Corticosterone ◽  
Weanling Rats ◽  
Pituitary Glands ◽  
Hypophysectomized Rats ◽  
Normal Controls ◽  
Donor Source

ABSTRACT Hypophysectomized female weanling rats were transplanted with heterotrophic pituitary glands removed from male and female virgin and breeder rats. The virgin rats were normal whereas the breeder rats had varying degrees of arteriosclerosis, hypertension, diabetes, and other degenerative diseases. The multiple ectopic pituitary glands, regardless of donor source, were equally effective in maintaining growth, thymus, adrenal, heart, kidney, and ovarian weight and serum corticosterone levels well above the hypophysectomized controls but not equal to normal controls. Histological evidence rather than gravimetric or serum corticosterone data suggests that the pituitary glands of repeatedly bred female rats may contain extra gonadotrophic and adrenocorticotrophic activity.

Influence of manganese on susceptibility of rats to convulsions

1963 ◽  
Vol 204 (3) ◽  
pp. 493-496 ◽  
Author(s):  
Lucille S. Hurley ◽  
Dorothy E. Woolley ◽  
Fred Rosenthal ◽  
Paola S. Timiras
Keyword(s):  
Brain Function ◽  
The Body ◽  
Manganese Deficiency ◽  
Convulsive States ◽  
Eeg Recordings ◽  
Manganese Salts ◽  
Relationship Of ◽  
The Relationship ◽  
Prior Administration ◽  
Normal Controls

The relationship of manganese to some aspects of brain function was studied in rats. Electroshock convulsions were produced in the following groups: 1) normal controls, 2) manganese-deficient, not ataxic, 3) manganese-deficient, congenitally ataxic, 4) not manganese-deficient, congenitally ataxic. The threshold for minimal seizures was significantly lower than normal in the two manganese-deficient groups. All manganese-deficient rats also showed alterations in the pattern of a maximal seizure. These data are interpreted to mean that brain excitability or convulsability was increased in manganese-deficient rats regardless of the presence or absence of ataxia, thus suggesting that congenital ataxia and increased convulsability are independent expressions of manganese deficiency. The convulsions and death induced by l-hydrazinophthalazine (hydralazine) in normal rats could be prevented by the prior administration of manganese salts. Cortical electroencephalographic (EEG) recordings indicated that ataxic manganese-deficient animals have a higher average EEG frequency under anesthesia than do controls. These studies suggest that the level of manganese in the body is important in determining the susceptibility of an animal to convulsive states.

Effects of hypophysectomy and dexamethasone on rat adrenal response to microwaves

1979 ◽  
Vol 47 (6) ◽  
pp. 1284-1288 ◽  
Author(s):  
W. G. Lotz ◽  
S. M. Michaelson
Keyword(s):  
Plasma Corticosterone ◽  
Acth Secretion ◽  
Microwave Exposure ◽  
Hypophysectomized Rats ◽  
Integrative Process ◽  
Corticosterone Response ◽  
Adrenal Response ◽  
Prior Administration ◽  
Stimulation Of ◽  
Intact Rats

Circulating corticosterone levels were measured to compare the adrenocortical response to acute microwave exposure of normal, hypophysectomized, or sham-hypophysectomized rats. Plasma corticosterone levels in acutely hypophysectomized rats exposed to 60 mW/cm2 for 60 min were below control levels, indicating that the microwave-induced corticosterone response observed in normal, intact rats is dependent on ACTH secretion by the pituitary. In other groups of rats pretreated with dexamethasone before being exposed to microwaves for 60 min, the corticosterone response to a 50-mW/cm2 exposure was completely suppressed by doses equal to or greater than 3.2 micrograms dexamethasone/100 g body weight. However, the corticosterone response to a 70-mW/cm2 exposure was only partially suppressed by prior administration of 3.2 or 5.6 micrograms dexamethasone/100 g BW. The evidence obtained in these experiments, in conjunction with the results of other experiments previously reported, is consistent with the hypothesis that the stimulation of the adrenal axis in the microwave-exposed rat is a systemic, integrative process due to a general hyperthermia.

The Steroid Feedback Mechanism

1957 ◽  
Vol 192 (1) ◽  
pp. 58-62 ◽  
Author(s):  
Shawn Schapiro ◽  
Jessie Marmorston ◽  
Harry Sobel
Keyword(s):  
Carotid Artery ◽  
Feedback Mechanism ◽  
Blood Levels ◽  
Acth Secretion ◽  
Cerebral Structure ◽  
Hypophysectomized Rats ◽  
Intact Rats

The mechanism whereby high blood levels of the adrenal cortical hormones inhibit the secretion of ACTH following stress has been investigated. The 4-hour change in circulating eosinophils was used as criterion for ACTH secretion. DCA administration into intact rats prevented the endogenous mobilization of ACTH following stress. When the venous brain blood from the stressed hypophysectomized rat was injected into these DCA-treated intact rats, a discharge of ACTH occurred in the recipients as indicated by a pronounced 4-hour eosinopenia. Carotid artery blood from stressed hypophysectomized rats was relatively inactive in provoking ACTH secretion when injected into intact DCA-treated recipients. If DCA is administered to the hypophysectomized donor rat, its brain blood contains no, or only slight, pituitary stimulating activity. It is concluded that at least one mechanism whereby high levels of the adrenal cortical hormones inhibit the release of ACTH following stress is by blocking the secretion from a cerebral structure, presumably the hypothalamus, of a pituitary stimulating substance (s).

Optimization of Heparin Anticoagulation during Membrane Plasma Separation

1988 ◽  
Vol 11 (4) ◽  
pp. 313-316 ◽  
Author(s):  
G.M. Frascà ◽  
A. Buscaroli ◽  
L.C. Borgnino ◽  
A. Vangelista
Keyword(s):  
Plasma Exchange ◽  
Plasma Flow ◽  
Distribution Volume ◽  
Blood Levels ◽  
Heparin Concentration ◽  
Sieving Coefficient ◽  
Heparin Anticoagulation ◽  
Membrane Plasma Separation ◽  
The Individual ◽  
Heparin Dosage

This study analyses 75 membrane plasma exchanges carried out in 18 patients where various amounts of heparin were used to define the heparin kinetic during plasma exchange and the appropriate anticoagulation. A specific assay was employed to measure heparin concentration. Our results showed that: 1) the heparin distribution volume exceeded the expected value by 10 to 25%; 2) the drug is filtered with a sieving coefficient = 1; 3) the appropriate concentration range is within 0.2 and 0.5 Ul/ml.; 4) the heparin blood levels strictly correlate with a PTT (p<0.001); 5) the individual need for heparin is related to the patient Hct (p<0.001) and plasma flow (p<0.001). Simple quidelines are provided to determine the appropriate heparin dosage in single patients.

Role of Hypophysis and Adrenals in Fatty Infiltration of Liver Resulting From Acute Ethanol Intoxication

1955 ◽  
Vol 184 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Samuel Mallov ◽  
Janet L. Bloch
Keyword(s):  
Liver Lipid ◽  
Fatty Infiltration ◽  
Female Rats ◽  
Ethanol Intoxication ◽  
Lipid Response ◽  
Acute Ethanol ◽  
Hypophysectomized Rats ◽  
Acute Ethanol Intoxication ◽  
Prior Administration

Acute ethanol intoxication was found to promote the fatty infiltration of liver in rats. The liver lipid concentrations gradually rose to peak values, then slowly returned to normal. The duration of the fatty infiltration, and the peak liver lipid values obtained, were functions of the dose of ethanol administered. Female rats showed a more severe fatty infiltration than did males, under the same conditions. The prior administration of large quantities of choline reduced the intensity of the fatty infiltration provoked by the ethanol. In contrast to intact animals, neither adrenalectomized nor hypophysectomized rats showed an accumulation of liver lipids as a result of acute ethanol intoxication. Adrenalectomized rats maintained on cortisone, and adrenal demedullated rats, however, showed the same liver lipid response to ethanol as did intact rats. Rats chronically intoxicated for a period of 30 days exhibited hypertrophy of the adrenals. Acute intoxication produced by isopropanol administration also resulted in the accumulation of liver lipid. It is suggested that ethanol intoxication may cause the mobilization of fat from the depots to the liver, and that pituitary and adrenal cortical hormones are involved in the mechanism of this mobilization.

Pharmacokinetics of Paracetamol, Diclofenac and Vidarabine during Plasma Exchange

1988 ◽  
Vol 11 (3) ◽  
pp. 195-200 ◽  
Author(s):  
F. Fauvelle ◽  
A. Leon ◽  
M.T. Niakate ◽  
O. Petitjean ◽  
L Guillevin
Keyword(s):  
Protein Binding ◽  
Plasma Exchange ◽  
High Performance ◽  
Plasma Clearance ◽  
Distribution Volume ◽  
Volume Distribution ◽  
Binding Characteristics ◽  
Low Protein ◽  
B Virus ◽  
Large Distribution

In order to establish guidelines for prescribing drugs in patients treated with plasma exchange (PE), we studied the pharmacokinetics of paracetamol (5 patients), diclofenac (4 patients) and vidarabine (3 patients) during one or several PE. Results were compared with those obtained without PE. Diclofenac and paracetamol were choosen because they presented different volume distribution and protein binding characteristics. Vidarabine was studied because we use it for the treatment of patients with polyarteritis nodosa related to hepatitis B virus. Diclofenac (100 mg) and paracetamol (1000 mg) were given 1 hour before PE. Samples were obtained 60 and 30 min before PE, every 15 min during PE and hourly for 2 hours after the end of PE. Vidarabine was given in continuous infusion, 15 mg/kg/d during the first week of treatment and 7.5 mg/kg/d during subsequent weeks. Samples were obtained before PE, 3 times during PE and every 30 min for 4 hours after the end of PE. Paracetamol, diclofenac, vidarabine and hypoxanthine arabinoside were assayed by high performance liquid chromatography. During each PE 60 ml/kg were removed and replaced by albumin. We found that 17% of diclofenac, 4.3% of paracetamol and 4.9% of vidarabine were removed during each session. Plasmapheresis clearance was 51% of plasma clearance for diclofenac, 15% for paracetamol and 10% for vidarabine. Drugs which are mainly removed during PE are those which are bound to proteins with a small distribution volume. Those drugs, such as diclofenac, must be administered after the end of each PE session. Drugs which present a large distribution volume and low protein binding can be given before the session. Vidarabine can be administered during PE without loss of effectiveness due to drug removal.

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