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Biomedical subjects

J W Ensinck

Publications and source records attributed to J W Ensinck.

104 records · Page 6Linked to original sources
PubMed1968

The nature of human serum insulin-like activity (ILA)P Characterization of ILA in serum and serum fractions obtained by acid-ethanol extraction and adsorption chromatography.

Studies were undertaken in an attempt to clarify the apparent heterogeneous nature of human serum insulin-like activity. Methods of preparative zone electrophoresis on Pevikon, acid-ethanol extraction of trichloroacetic acid serum protein precipitates, adsorption chromatography on DEAE-cellulose and Dowex 50, gel filtration chromatography, and insulin antiserum immunoreactivity were used. The results establish the presence of a substance in serum with in vitro biological properties similar to insuln but with different physicochemical properties. The major portion of serum ILA measured by bioassay techniques can be attributed to the effects of this substance. Whereas the in vitro biological effects of this substance on muscle and adipose cells were similar to those of crystalline insulin, the substance is distinguished from insulin by: (1) the failure of insulin antiserum to inhibit its in vitro biological effect; (2) a slower electrophoretic mobility (in the gamma-beta globulin zone); and (3) a larger molecular weight, between 40,000 and 50,000 in these studies. It is similar to insulin since both are soluble in acid-ethanol. The results further indicate that previously described insulin-like activity in gamma-beta globulin preparations, the major portion of total serum insulin activity described in acid-ethanol extracts of serum, "bound" insulin, "atypical" insulin, and antibody nonsuppressible insulin-like activity bioassayed in diluted serum are all one and the same substance.

Adipose Tissue↗
PubMedDate not supplied

Somatostatin in epithelial cells of intestinal mucosa is present primarily as somatostatin 28.

Region-specific antisera to [Tyr14]-SS28(1-14) were used to identify cells containing immunoreactivity to the SS28(1-14) fragment of somatostatin 28 (SS28) in gastric and intestinal mucosal epithelium and in pancreatic islets by immunoperoxidase staining. Radioimmunoassay with iodinated [Tyr14]-SS28(1-14) identified one antiserum (F4) to SS28(1-14) that cross-reacted equally with SS28(1-12), SS28(1-14) and SS28. Two other antisera (F3 and F8) to SS28(1-14) did not cross-react with SS28(1-12) and showed insignificant cross-reactivity to SS28. Immunostaining results showed that F4 stained the same cells that reacted with antiserum AS-10, which is specific for the cyclic tetradecapeptide somatostatin, SS28(15-28). Antisera F3, F4, and F8 all reacted with islet D cells and with somatostatin cells in the antral mucosa. However, only antiserum F4 detected immunoreactivity in mucosal epithelial cells; F3 and F8 did not bind to these cells. After sections of intestine were exposed to trypsin, however, epithelial cells containing immunoreactivity to SS28(1-14) were detected in intestinal mucosa with antisera F3 and F8. These results were obtained for duodenum, jejunum, ileum, and colon, but most of the epithelial cells with immunoreactivity to SS28(1-14) were in the duodenum. Both radioimmunoassay and immunostaining results suggest that F3 and F8 bind to a region of SS28(1-14) that is unavailable to antibodies in the intact SS28 molecule.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Insulin responses to glucose in non-insulin-dependent diabetic subjects with and without the chlorpropamide-alcohol flush: effect of salicylate and naloxone.

We examined the role of endogenous opiates and/or prostaglandins on the abnormal insulin secretion characteristic of some non-insulin-dependent diabetic subjects. A group of chlorpropamide-alcohol flush positive (CPAF+) and a group of flush negative (CPAF-) non-insulin-dependent subjects were compared as to their pancreatic beta-cell responses to intravenous glucose tolerance tests before and after sodium salicylate infusion, and before and after naloxone infusion. There was no difference in mean insulin secretion (either first or second phase) between CPAF+ versus CPAF- groups. Both groups increased their insulin secretion with salicylate infusion, and both had a small decrease with naloxone infusion. There was no correlation between chlorpropamide-alcohol flushing and beta-cell response to glucose.

Adult↗
PubMedDate not supplied

Autonomic neural dysfunction in recently diagnosed diabetic subjects.

Because onset of autonomic neural dysfunction in the diabetic syndrome has not been well established, sensitive and quantitative measures of autonomic nervous system (ANS) function were made in 19 non-insulin-dependent (NIDD) and 14 insulin-dependent (IDD) recent-onset diabetic subjects. The known duration of diabetes mellitus in the NIDD subjects was less than or equal to 12 mo. The duration in the IDD subjects was less than or equal to 24 mo. RR-variation during beta adrenergic blockade (an index of an ANS reflex involving the cardiac parasympathetic nervous system [PNS] pathway) was smaller than that of control subjects in both NIDD (P less than 0.001) and IDD subjects (P less than 0.01). This PNS abnormality was not likely to be due to volume depletion since acute volume depletion induced by furosemide in six normal subjects (1608 +/- 105 ml, mean +/- SEM) did not change RR-variation. Dark-adapted pupil size after topical PNS blockade (an index of iris sympathetic nervous system [SNS] activity) was also smaller in both groups of diabetic subjects (NIDD, P less than 0.01; IDD, P less than 0.05). Pupillary latency time (an index of an ANS reflex involving iris PNS pathway) was prolonged in the NIDD subjects (P less than 0.005) but was not significantly altered in the IDD subjects. Thus, it would appear that the ANS is impaired soon after the diagnosis of diabetes mellitus. We hypothesize that early impairment of the ANS is common in IDD and NIDD subjects. This finding is consistent with the hypothesis that abnormal carbohydrate metabolism is an important factor in the etiology of diabetic autonomic neuropathy.

Adult↗