Influence of the vitamin D-binding protein on the serum concentration of 1,25-dihydroxyvitamin D3. Significance of the free 1,25-dihydroxyvitamin D3 concentration.

The influence of the serum binding protein (DBP) for vitamin D and its metabolites on the concentration of its main ligands, 25-hydroxyvitamin D(3) (25-OHD(3)) and 1,25-dihydroxyvitamin D(3) (1,25-[OH](2)D(3)) was studied. The concentration of both 1,25-(OH)(2)D(3) and DBP in normal female subjects (45+/-14 ng/liter and 333+/-58 mg/liter, mean+/-SD, respectively; n = 58) increased during the intake of estro-progestogens (69+/-27 ng/liter and 488+/-90 mg/liter, respectively; n = 29), whereas the 25-OHD(3) concentration remained unchanged. A positive correlation was found between the concentrations of 1,25-(OH)(2)D(3) and DBP in these women. At the end of pregnancy, the total concentrations of 1,25-(OH)(2)D(3) (97+/-26 ng/liter, n = 40) and DBP (616+/-84 mg/liter) are both significantly higher than in nonpregnant females and paired cord serum samples (48+/-11 ng/liter and 266+/-41 mg/liter, respectively). A marked seasonal variation of 25-OHD(3) was observed in pregnant females and their infants, whereas in the same samples the concentrations of both DBP and 1,25-(OH)(2)D(3) remained constant throughout the year. The free 1,25-(OH)(2)D(3) index, calculated as the molar ratio of this steroid and DBP, remains normal in women taking estro-progestogens, however, and this might explain their normal intestinal calcium absorption despite a high total 1,25-(OH)(2)D(3) concentration. In pregnancy the free 1,25-(OH)(2)D(3) index remains normal up to 35 wk of gestation, but during the last weeks of gestation, the free 1,25-(OH)(2)D(3) index increases in both circulations. A highly significant correlation exists between the (total and free) 25-OHD(3) and 1,25-(OH)(2)D(3) concentrations in maternal and cord serum both at 35 and 40 wk of gestation.

Vitamin D metabolites and their binding protein in adult diabetic patients.

Vitamin D metabolites and vitamin D-binding protein were measured in the serum of nonketotic Bantu and Caucasian insulin-requiring diabetic subjects from Zaire and Belgium, respectively. In Caucasian diabetics, whether untreated (N = 18) or insulin treated (N = 26), no abnormalities were found. The Bantu diabetics (N = 20) were more insulin-deficient and had a poorer glucose control than the Caucasians. They presented, compared with Bantu controls, a significant decrease in the serum concentrations of 25-hydroxyvitamin D3 (26 +/- 10 vs. 35 +/- 14 micrograms/L, P less than .01), 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] (38 +/- 15 vs. 58 +/- 17 ng/L, P less than .001), and vitamin D-binding protein (303 +/- 55 vs. 356 +/- 41 mg/L, P less than .001). The decreased concentrations of vitamin D metabolites in the adult Bantu diabetic patients may be partly explained by a concomitant decrease in the concentration of vitamin D-binding protein, possibly due to insulin deficiency. The ratio between the molar concentrations of 1,25-(OH)2D3 and vitamin D-binding protein, used as an index of the free hormonal level, was also decreased, in association with a decreased serum calcium level. In conclusion, no abnormalities in vitamin D metabolism were found in Caucasian insulin-dependent diabetics, whereas low serum 1,25(OH)2D3 concentrations and hypocalcemia were found in poorly controlled Bantu diabetic subjects.

Secretion of prostatic binding protein by rat ventral prostate: influence of age and androgen.

Rat ventral prostate of adult male rats contain a large amount of prostatic binding protein (PBP). Immunological evidence indicates that this protein is a specific secretion product of this gland. The amount and concentration of PBP in ventral prostate show marked changes as a function of age. PBP is low but detectable (0.009 and 0.002 U/mg prostate) in 5- and 10-day-old rats and increases thereafter in a biphasic way to adult levels (0.619 U/mg prostate). After castration of PBP drops to 0.054 U/mg prostate after 10 days and 0.030 U/mg prostate after 21 days. The concentration of PBP returns to precastration levels after 2 weeks of androgen treatment. Estradiol and progesterone are ineffective in this respect. The antiandrogen, cyproterone acetate, counteracts the stimulatory effect of testosterone propionate.

Influence of vitamin D status on insulin secretion and glucose tolerance in the rabbit.

The influence of vitamin D status on insulin secretion and glucose tolerance was studied by a longitudinal design in the rabbit. Intravenous glucose tolerance tests were performed in Dutch rabbits (n = 12) before and after nutritional vitamin D deficiency, characterized by an absence of circulating 25-hydroxyvitamin D3, a 50% decrease in 1,25-dihydroxyvitamin D3, and a 16% decrease in serum calcium concentrations. Glucose-induced insulin secretion was reduced by 41% as early as 2 months after the start of the vitamin D-deficient diet and was associated with an impairment of glucose tolerance. An iv calcium infusion restored the serum calcium concentration of the vitamin D-deficient rabbits (n = 5), but did not improve glucose-mediated insulin secretion. When these animals received a single ip injection of 100 ng 1,25-dihydroxyvitamin D3 10 h before the glucose test, their insulin responses significantly increased. Supplementation with 25-hydroxyvitamin D3 for 2 weeks in another group of rabbits (n = 4) resulted in marked improvement in glucose-stimulated insulin release and glucose tolerance. These results show that vitamin D affects glucose-induced insulin secretion by a mechanism that involves more than its regulating action on serum calcium concentration.

Lack of effect of the vitamin D status on the concentration of the vitamin D-binding protein in rat serum.

The influence of the vitamin D status on the concentration of the serum vitamin D-binding protein was studied. In normal rats the serum vitamin D-binding protein increases gradually from birth to adulthood; after puberty a higher concentration is found in male rats than in female rats. Rats fed a vitamin D-deficient diet containing a sufficient amount of calcium and phosphorus were found to have a normal DBP (binding protein for vitamin D and its hydroxylated metabolites) pattern indistinguishable from that of rats receiving the same diet but supplemented with a weekly injection of 500 microgram vitamin D3. Rats fed a vitamin D-deficient, low calcium, low phosphorus diet developed severe hypocalcemia and growth retardation, but their DBP pattern was not significantly different from that of rats fed the same diet but supplemented with a weekly injection of 500 microgram vitamin D3. The concentration of the transport protein for vitamin D was thus unrelated to the vitamin D status of the rat.

Immunochemical measurement of the vitamin D-binding protein in rat serum.

The vitamin D-binding protein (DBP) was measured in rat serum using a single radial immunodiffusion technique. Normal serum levels at birth (74 +/- 11 mg/liter, mean +/- SD) were lower than during the last day of fetal life (130 +/- 14 mg/liter) and much lower than in adult rats. A marked sex difference in DBP occurred after puberty: male values (656 +/- 52 mg/liter) were significantly higher than female values (472 +/- 46 mg/liter). The sex difference could be abolished by either adult gonadectomy or transpharyngeal hypophysectomy. Implantation of a pituitary gland under the renal capsule in hypophysectomized male rats further decreased the DBP concentration, suggesting that PRL suppresses the DBP level. A similar decrease was also observed at the end of pregnancy and during lactation. Administration of androgens to either normal female or gonadectomized male rats increased their DBP concentration to the normal adult male level. The serum levels of total 25-hydroxyvitamin D did not fluctuate according to the concentration of DBP, indicating that the concentration of "free 25-hydroxyvitamin D" is not regulated at a constant level.

1,25-Dihydroxyvitamin D and vitamin D-binding protein are both decreased in streptozotocin-diabetic rats.

Calcium and vitamin D metabolism were studied in streptozotocin-treated rats up to 10 days after the induction of diabetes. Proteinuria, hypercalciuria, and hyperphosphaturia appeared as early as 3 days after diabetes induction and were reversed by insulin. The serum proteins and fasting calcium concentrations were decreased in untreated diabetic rats. The concentration of serum vitamin D binding protein (DBP) was higher in male than in female control rats (mean +/- SD; 555 +/- 73 vs. 348 +/- 28 mg/liter, P less than 0.001). When sequentially measured in male untreated diabetic rats, DBP concentration steadily decreased. Compared with control values, DBP was reduced 19%, 28%, and 32% on days 3, 6, and 10, respectively, after induction of diabetes in male rats. In female animals, DBP was reduced 22% on day 10 of diabetes. DBP concentration was corrected by insulin treatment of diabetic rats and remained normal in streptozotocin-treated animals that did not develop diabetes. The serum concentration of 25-hydroxyvitamin D3 was similar in both sexes and was not affected by diabetes. Like DBP, the concentration of total 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] was higher in male than in female control rats (120 +/- 24 vs. 96 +/- 17 ng/liter, P less than 0.001), but 10 days after induction of diabetes this concentration decreased by 37% and 29% in male and female rats, respectively. The free 1,25-(OH)2D3 concentration, estimated from the molar 1,25-(OH)2D3/DBP ratio, was similar in both sexes and was not decreased by diabetes. We conclude that experimental diabetes in the rat induces a decrease in DBP concentration and a concomitant decrease in total but not in free 1,25-(OH)2D3 concentrations. This may indicate that diabetes decreases circulating 1,25-(OH)2D3 concentrations through alterations in DBP levels.

Association of aberrant transcortin levels with HLA antigens of the B and C loci: high transcortin levels are frequently found in patients with lymphatic leukemia, hairy cell leukemia, or non-Hodgkin lymphoma.

HLA antigen B12 is in linkage disequilibrium with HLA antigen Cw5. In some way this particular haplotype seems to be associated with a mechanism increasing serum transcortin levels. As shown before, the latter mechanism does not involve elevated estrogen levels or a generalized increase in glycoprotein synthesis. Similar high transcortin levels (more than 2 SDs above the mean) are found frequently in patients with lymphatic leukemia, hairy cell leukemia, or non-Hodgkin lymphoma, as well as in the siblings of these patients. HLA antigen Bw35 is in linkage disequilibrium with HLA antigen Cw4. Transcortin levels in patients with this combination of HLA antigens are significantly lower than in patients who do not carry these two antigens. Relatives of subjects with very low transcortin levels often have the same low levels. These findings together with recent data in the literature suggest that a cluster of genes regulating certain aspects of glucocorticoid metabolism is located in the vicinity of HLA locus B and C.

Influence of thyroid function on the serum concentration of 1,25-dihydroxyvitamin D3.

The serum concentrations of parathyroid hormone, 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 were measured in patients with untreated thyroid disorders. The serum concentration of parathyroid hormone was decreased in hyperthyroidism [20 +/- 10 mU/liter, (mean +/- SD); n =23; P < 0.01] and increased in hypothyroidism (53 +/- 17 mU/liter; n = 12; P < 0.001) compared to that in normal subjects (26 +/- 9 mU/liter; n = 81). The concentration of 25-hydroxyvitamin D3 was not altered, but the concentration of 1,25-dihydroxyvitamin D3 was significantly lower in the serum of hyperthyroid patients (28 +/- 11 ng/liter) than in the serum of normal subjects (42 +/- 13 ng/liter). On the contrary, an increased concentration of 1,25-dihydroxyvitamin D3 was observed in the serum of hypothyroid patients (73 +/- 28 ng/liter; P < 0.001 vs. normal subjects). The abnormal serum concentrations of 1,25-dihydroxyvitamin D3 in thyroid disorders cannot be explained by differences in serum binding because the serum vitamin D-binding protein was unaltered in hyperthyroid subjects and only slightly increased (+17%) in hypothyroid subjects. These changes in the serum concentration of 1,25-dihydroxyvitamin D3 are compatible with previous data on altered intestinal calcium absorption in thyroid disorders.

25-hydroxyvitamin D and its binding protein in maternal and cord serum.

Serum calcium, phosphorus, albumin, total protein, 25-hydroxyvitamin D (25OHD) and the vitamin D-binding protein (DBP) were measured in 30 cord sera and in 30 sera obtained simultaneously from their respective mothers. The maternal serum concentration of 25OHD (14.0 +/- 6.9 microgram/l, mean +/- SD) and of DBP (574 +/- 72 mg/l) were significantly higher than the respective cord serum concentration (8.0 +/- 4.4 microgram/l and 268 +/- 39 mg/l). The calculated concentration of "free 25OHD," however, was slightly but significantly higher in cord serum (0.44 +/- 0.24 ng/l) than in maternal serum (0.34 +/- 0.18 ng/l). Serum calcium and phoshporus were lower in maternal than in cord serum. A highly significant positive correlation was found between maternal and cord serum concentration of DBP (r = 0.59), total 25OHD (r = 0.79), "free 25OHD" (r = 0.86) and phosphorus (r = 0.73). These data indicate that the concentration of DBP is important for the evaluation of the placental transfer of 25OHD. Indeed, the concentration of "free 25OHD" is slightly higher in cord serum than in maternal serum, despite the maternal-to-fetal gradient of total 25OHD. The low fetal concentration of DBP is also unfavorable for the fetal storage of 25OHD during intrauterine life.

The measurement of the vitamin D-binding protein in human serum.

The concentration of the vitamin D-binding protein was measured in human serum by single radial immunodiffusion. Normal serum concentrations were slightly higher in normal women than in normal men. No race-related difference was found between white people from Belgium and black people from Zaire. Lower concentrations were found in cord serum and in patients with cirrhosis of the liver. Increased serum levels were observed during pregnancy or during the intake of estro-progestogens. The serum level of the vitamin D-binding protein was not altered in various diseases of calcium metabolism (primary osteoporosis, primary and secondary hyperparathyroidism, rickets, osteomalacia or vitamin D intoxication). No correlation was found between serum levels of 25-hydroxy vitamin D and those of its binding protein. From these data the following conclusions can be drawn: 1) The serum concentration of the vitamin D-binding protein (about 6.10(-6)M) largely exceeds the normal serum concentration of 25-hydroxy vitamin D (about 4.10(-8)M), so that this protein is normally for less than 1% saturated, 2) Normal serum levels of the vitamin D-binding protein were observed in several diseases of calcium metabolism, and 3) The free concentration of 25-hydroxyvitamin D is not regulated at a constant level.

The effect of anticonvulsant therapy on serum levels of 25-hydroxy-vitamin D, calcium, and parathyroid hormone.

In 20 female patients treated for 2 to 37 years (mean :12) with anticonvulsant drugs, low serum levels of 25-hydroxy-vitamin D (25-OH-D; 6.4 +/- 3.2 ng/ml M +/- SD), relative hypocalcemia (9.2 +/- 0.4 mg/100 ml) and high levels of parathyroid hormone (PTH 277 +/- 165 pg/ml) were found compared to an age-matched control group (respectively 8.6 +/- 3.2 ng/ml, 9.6 +/- 0.3 mg/100 ml and 183 +/- 95 pg/ml) living in the same psychiatric clinic. A significant negative correlation was found between total duration of treatment and either serum 25-OH-D or serum calcium. After treatment with an oral vitamin D3 supplement (2000 IU/day) for 3 weeks, the serum 25-OH-D levels, although increased, remained lower than normal in the epileptic group and neither hypocalcemia nor their secondary hyperparathyroidism were corrected. These data confirm the occurrence of vitamin D deficiency in patients treated with anticonvulsant drugs resulting in hypocalcemia and secondary hyperparathyroidism.

Serum vitamin D metabolites and their binding protein in patients with liver cirrhosis.

Serum parameters of calcium metabolism were measured in 32 consecutive patients with biopsy-proven cirrhosis due to either hepatitis (n = 13), alcohol abuse (n = 11), Wilson's disease (n = 3), or primary or secondary biliary cirrhosis (n = 5). All measurements were normal in the small group of patients with Wilson's disease. The serum concentrations of albumin, vitamin D-binding protein, total calcium, phosphorus, and 1,25-dihydroxyvitamin D3 (1,25-(OH2)D3) were decreased in the other patients with cirrhosis, but their mean serum concentrations of ionized calcium, 25-hydroxyvitamin D3 (25-OHD3) and free 1,25-(OH2)D3 index were normal. A slight but significant increase in the serum PTH measured using a carboxyl-terminal antiserum was found. A significant correlation was found between the serum concentration of either albumin or vitamin D-binding protein and the serum concentrations of total calcium, 25-OHD3, 1,25-(OH2)D3, and PTH but not with ionized calcium or free 1,25-(OH2)D3 index. The observed abnormalities of calcium metabolism in unselected patients with cirrhosis were mainly due to decreased protein synthesis. Only the patients with severe cirrhosis had decreased concentrations of 25-OHD3 but they were nevertheless able to maintain a normal ionized serum calcium and free 1,25-(OH2)D3 level, possibly by means of compensatory hyperparathyroidism.

Serum lipids and apolipoproteins A-I, A-II, and B in hyperthyroidism before and after treatment.

The serum concentrations of total cholesterol (TC), triglycerides (RG), high density lipoprotein-cholesterol (HDLc), low density lipoprotein-cholesterol (LDLc), and the apolipoproteins (apo) A-I, A-II, and B were measured in 33 hyperthyroid patients before and after treatment. The results were compared with those of healthy controls. Apo A-I, A-II, and B were assayed by immunonephelometry. The serum levels of TC (mean +/- SD, 167 +/- 36 mg/dl, HDLc (40.8 +/- 12 mg/dl), and LDLc (108 +/- 35 mg/dl) were decreased in the untreated hyperthyroid patients compared to both the values after treatment (TC: 215 +/- 54 mg/dl; P less than 0.001; HDLc: 52 +/- 14 mg/dl; P less than 0.001; LDLc: 146 +/- 47 mg/dl; P less than 0.001) and the control values (TC: 206 + 39 mg/dl; P less than 0.001; HDLc: 47.4 +/- 10 mg/dl; P les than 0.01; LDLc: 145 +/- 38 mg/dl; P less than 0.001). TG levels were not statistically different before and after treatment. The apo A-I concentrations (116 +/- 24 mg/dl) were lower before than after treatment (131 +/- 28 mg/dl; P less than 0.01), but they were not statistically different from those in the control group (115 +/- 19 mg/dl). The apo A-II levels were identical in all groups (before treatment, 35 +/- 7 mg/dl; after treatment, 37 +/- 9 mg/dl; control group, 36 +/- 9 mg/dl). The apo B levels were lower in the untreated hyperthyroid patients (86 +/- 23 mg/dl) compared to those in controls (103 +/- 19 mg/dl; P less than 0.001) and patients after therapy (103 +/- 25 mg/dl; P less than 0.001). The increase in HDLc relative to the major HDL apo A-I and A-II during treatment for hyperthyroidism was associated with changes in body weight. The apo A-I to apo A-II and LDLc to apo B ratios, however, were significantly lower before compared to those after treatment, when the influence of increasing body weight during therapy was accounted for. This study emphasizes the important regulating role of thyroid hormones on lipid and apolipoprotein metabolism.

Unexplained high transcortin levels in patients with various hematological disorders and in the relatives: a connection between these high transcortin levels and HLA antigen B12.

Forty-one our of 141 patients with various hematological disorders had serum transcortin values more than 2 sDs above the normal mean (relative risk vs. controls, 10.78). Their relatives also had a higher incidence of unusually high transcortin values. The serum levels of steroid-binding beta-globulin were normal in these patients as well as in their relatives, making an increase in estrogenic impregnation as the cause of the high transcortin levels most improbable. Other known causes of increased transcortin levels could also be excluded. Such unusually high transcortin levels are 4.74 times more frequent in subjects carrying an HLA antigen B12 than in a control group [P (corrected) less than 0.006]. However, the HLA antigen B12 and hematological disorders were independently associated with high transcortin levels.

Secretion rates of LH and FSH during infusion of LH-FSH/RH in normal women and in patients with secondary amenorrhea: suggestive evidence for two pools of LH and FSH.

Normal women in the early follicular phase and in the luteal phase of the cycle, and patients with secondary amenorrhea received on consecutive days a rapid intravenous injection (50 mug) and a two or four-hour infusion (25 mug/h) of synthetic LH-FSH/RH. The responses of LH and FSH were evaluated by the measured plasma concentrations, as well as by the calculated pituitary secretion rates and by the amounts of hormone released. To estimate these pituitary secretion rates of LH and FSH, a simplified mathematical model is proposed. During an infusion of LH-FSH/RH the secretion rates of both LH and FSH increased in the three groups of women in a biphasic way with a dip after 1 to 2h of infusion, suggesting that besides the pool mobilized by a rapid intravenous injection of LH-FSH/RH there is a second pool of (stored) gonadotropins. For LH the increase above baseline concentrations was higher in group II (luteal phase) than in group I (follicular phase) or in group III (amenorrhea) and this both after a bolus injection and during infusion of LH-FSH/RH. For FSH a similar pattern of response prevailed during an infusion of LH-FSH/RH. After a bolus administration, however, the FSH release was relatively higher in group III (amenorrhea) than in both groups of normal women in which the increases were about the same. The latter finding suggests that the first pool of FSH is released by a different mechanism than the second pool.

Hyperthyroidism influences the distribution and apolipoprotein A composition of the high density lipoproteins in man.

Hyperthyroidism has a different influence on the major high density lipoprotein (HDL) components cholesterol, apoprotein (apo) A-I, and apo A-II. To characterize in greater detail the alterations induced by hyperthyroidism within the HDL subclasses, we investigated HDL distribution and composition in 11 hyperthyroid women before and during treatment. The plasma concentrations of total cholesterol, HDL cholesterol, phospholipids, apo A-I, and apo B were decreased when the patients were hyperthyroid compared with the values during treatment. Apo A-II and apo C-III levels were only slightly lower in the hyperthyroid state. Triglyceride and apo E concentrations did not change significantly during therapy. Analysis of lipoprotein subclasses separated by isopycnic ultracentrifugation revealed 1) marked decreases in low density lipoprotein (LDL) cholesterol, phospholipids, and apo B; 2) less pronounced reductions in the very low density lipoprotein (VLDL) lipid and apo B concentrations; and 3) a consistent decrease in the HDL2b (density, 1.063-1.100 g/ml) fraction in the hyperthyroid patients. The reduction in HDL2b mass was associated with lower concentrations of HDL2b cholesterol, phospholipids, and apo A-I. The HDL2b apo A-II levels remained constant during treatment. Hyperthyroidism, therefore, modified the apo A composition of the HDL2b particles and resulted in a decreased molar apo A-I to apo A-II ratio within HDL2b. Further analysis of HDL particles differing in their apo A composition; i.e. HDL particles containing apo A-I only [(A-I)HDL] or containing both apo A-I and A-II [(A-I + A-II)HDL], by immunological procedures suggested that hyperthyroidism influenced the apo A content of HDL2b mainly by changing the proportions of (A-I)HDL and (A-I + A-II)HDL and the amount of apo A-I associated with (A-I)HDL. Treatment reversed the preferential decrease in (A-I)HDL within the HDL2b subclass. The particle sizes within HDL subfractions, measured by polyacrylamide gradient gel electrophoresis, were similar in the untreated and treated patients. Consequently, the decreased mass of apo A-I and lipids within HDL2b in the hyperthyroid patients could be attributed to a reduced number of identically sized particles within this fraction. These data demonstrate that the thyroid hormones are important regulators of HDL metabolism through their influence on the concentration and distribution of apo A-I.

Biochemical characterization of peritoneal fluid in women during the menstrual cycle.

Peritoneal fluid was collected at laparoscopy in women during the menstrual cycle and was assayed for protein and steroid hormone content. The total protein concentration in peritoneal fluid and the concentrations of the steroid hormone-binding proteins, transcortin and sex hormone-binding globulin, the polypeptide hormones, LH, FSH, and PRL, correlated with the plasma concentration but were lower; they were, respectively, 68%, 71%, 68%, 42%, and 34% of the plasma concentration. The concentrations of steroid hormones secreted by the ovary, i.e. 17 beta-estradiol, progesterone, androstenedione, and testosterone, were always equal or higher in peritoneal fluid than in plasma. In contrast, the concentrations of cortisol, a nonovarian steroid hormone, was 40% lower in peritoneal fluid than in plasma. No cyclic variations were observed in the peritoneal fluid concentrations of androstenedione and testosterone, two steroid hormones secreted by the stromal component of the ovary. On the contrary, the concentrations of 17 beta-estradiol and progesterone secreted by the follicular apparatus of the ovary increased sharply in peritoneal fluid after ovulation, reaching values of 44000 pg/ml and 3000 ng/ml, respectively. They declined progressively, whereas in plasma, peak concentrations were achieved only in the midluteal phase. In conclusion, the concentrations of 17 beta-estradiol and progesterone are much higher in peritoneal fluid than in plasma for at least 1 week after ovulation. We suggest that the secretion of the early, not yet vascularized, corpus luteum is directed preferentially toward the peritoneal cavity, creating a specific hormonal environment for the released oocyte and the oviduct.

Changes in some lipid variables in obese women during the early days of fasting.

Adult obese human subjects with a normal or slightly disturbed oral glucose tolerance test, were submitted to a 7-day fast. Initial serum triglyceride levels were inversely related to the Intralipid fractional removal rate, reflecting the close dependency of triglyceridemia on clearance efficiency; the correlation was less significant on the 5th day of fasting. The direction of the change in triglycerides during fasting was clearly related to the prefast triglyceride levels, the groups of patients with a lower level showing an increase, the group with a higher level showing a decrease. Changes in triglyceridemia were inversely related to fractional removal rate; changes in lipid clearing from plasma, however, could not explain the direction of changes in triglyceridemia in all subjects investigated. The group of patients responding to fasting with a decrease in triglyceridemia had a lower mean initial serum cholesterol value and their serum cholesterol levels showed a less prolonged increase during fasting than the other groups of patients.

More HLA haploidentity in pairs of sibs with the same transcortin levels.

In 50 sibships, each comprising at least 2 male sibs, the oldest sib was paired with each of his brothers. All sibs were HLA- haplotyped and their serum transcortin level was determined. The HLA haploidentical pairs were compared with the sibpairs having no HLA haplotype in common. The odds for the haploidentical pairs of having a small difference (less than 0.07 mg per g total serum protein) in serum transcortin was nearly 4 times (3.94; P less than 0.025) greater than for the pairs of brothers having no HLA haplotype in common. This abnormal distribution in HLA haplotypes confirms our previous findings on the relation of certain HLA haplotypes with either high or low basal serum transcortin levels.