No abstract

Since 1911 the problem of placental permeability to insulin has been studied sporadically. Carlson, Drennan, Orr and Jones (1, 2) observed that pregnant dogs failed to develop glycosuria after pancreatectomy and concluded that the fetus protected the mother against diabetes, presumably by diaplacental movement of some substance. Other investigators (3, 4), however, were unable to confirm these early studies. Results of work with goats (5), rabbits (6, 7) and mice (8) were variable and suggest that species differences exist in the placental permeability to insulin. By in vitro techniques, systems for the proteolytic inactivation of insulin have been demonstrated in the rat (9) and human placenta (10).This study was undertaken to investigate the role of the human placenta in the transfer and metabolism of insulin in vivo. It was assumed that the placenta handles insulin-I131 as it would unlabeled insulin. METHODTwenty-eight term-pregnant women, 14 to 41 years old, were chosen for this study without regard to parity. No diabetic patients were included. Except for two patients with mild pre-eclampsia (experiments 3 and 7), no complicating diseases were present. Four patients were delivered by elective repeat cesarean section (experiments 3, 7, 15, 16) with TCA due to losses of protein-bound radioactivity by adsorption to glass (10, 11). In subsequent experiments glass adsorption was minimized by using saline containing 0.5 per cent human serum albumin for the dilution of the labeled insulin.Several preparations of insulin-I.31 were analyzed by unidimensional descending chromatography on Munktell 20/150 filter paper (12) in butanol-acetic acid-water (3: 1: 4 or 8.5: 1: 7.5) after being supplemented with unlabeled carrier insulin, sodium iodide, L-monoiodotyrosine (MIT) and L-diodotyrosine (DIT). The iodinated carrier compounds were localized by staining with a solution of ceric sulfate-arsenious acid followed by aniline in acetone (13). Duplicate chromatograms were also sprayed with 0.1 per cent ninhydrin in acetone. The papers were cut into 1-to 2-cm segments and counted in a scintillation well counter. When detectable, the sum of the radioactivity migrating with the mobility of MIT and DIT was less than 1 per cent of the total radioactivity.

It has been known for many years that exercise decreases the insulin requirements of diabetics and increases glucose uptake from the blood even in untreated diabetic subjects. 1 Ingle 2 ' 3 demonstrated that severe work can cause a drop in blood sugar to extremely low levels in partially depancreatized diabetic rats receiving no insulin and that the effects of insulin and work are additive. Levine and his co-workers* investigated the effect of muscular work on the volume of distribution of nonmetabolizable monosaccharides in eviscerated, nephrectomized dogs and showed that exercise promotes the cellular entry of some sugars as does insulin. The sugars which respond to exercise in this preparation are those that also respond to insulin. Huycke and Kruhoffer 5 studied the perfused hindlimb preparation of the cat and observed that muscular exercise increases the rate of disappearance of D-glucose and D-galactose from the extracellular space. Helmreich and Cori 6 observed that tetanic contraction of skeletal muscle causes accumulation of free glucose within the muscle cells of intact animals. These authors 7 also compared the rate of penetration of infused pentoses into resting and exercising gastrocnemius muscles of nephrectomized rats. They found that pentoses penetrate the intracellular space of working muscles at an accelerated rate and that the effect of exercise parallels that of insulin. These results were recently confirmed in the cat by Sachs and his colleagues 8 who also noted the additive effect of insulin and exercise.These data demonstrate that exercise facilitates the entry of sugars into muscle cells. The mechanism of this action is essentially unknown. Levine and his coworkers* postulated that exercising muscle produces a humoral agent which accelerates the transfer of certain Presented by title at

No abstract

No abstract