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Biomedical subjects

M Langlois

Publications and source records attributed to M Langlois.

At least 91 records · Page 5Linked to original sources
PubMed1978

[Spontaneous hypoglycemia and chronic kidney insufficiency].

Although glucose intolerance occurs as a consequence of chronic renal failure, improvement of a diabetic state by deterioration of renal function is a well known phenomenon. Recently occasional cases of spontaneous hypoglycemia in patients with chronic renal failure have been reported; two such cases and the results of metabolic studies are described in this paper. Pituitary, thyroid and adrenal function appeared to be normal. The results of an oral glucose tolerance test were normal; an appropriate insulin response was demonstrated in one patient, and a slightly elevated basal insulin value with a delayed insulin response to oral administration of glucose was demonstrated in the other. An insulin tolerance test did not support the hypothesis of increased insulin sensitivity as a factor, and the growth hormone response to hypoglycemia was normal. An intravenous glucagon test caused a subnormal increase in plasma glucose concentration, and the intravenous administration of tolbutamide produced hypoglycemia without an increase insulin sensitivity as a factor, and the growth hormone response to hypoglycemia was normal. An intravenous glucagon test caused a subnormal increase in plasma glucose concnetration, and the intravenous administration of tolbutamide produced hypoglycemia without an increase in insulin values. The plasma alanine concentration was low and the proinsulin/insulin ratio was increased. The origin of this hypoglycemia is not clear but is probably multifactorial. However, low hepatic glycogen stores and inadequate gluconeogenesis due to substrate deficiency seem to be involved.

Adult↗
PubMed1978

[Ocular herpes : clinical variations and virus antigenic type (author's transl)].

Fifty-seven herpes simplex virus strains, isolated from ocular herpes, were screened by complement fixation, seroneutralization and thermosensitivity tests. They were distributed as follows : 44 type 1, 3 type 2, 7 intermediate type ; 3 had a type 2 thermosensitivity and a type 1 neutralization. Discrepancies in these results, with the three tests, show that there is, in each typed group, strains of virus which react differently, and this could indicate a continuity from one type to another. As the strain progressively reacts more like the type 2, clinical symptoms become more severe. In a certain number of cases where several simultaneous or successive samples were performed, there was a hypothetic possibility of change in the behaviour of herpes simplex virus strains in the eye.

Adolescent↗
PubMed1976

Comparison of the suppressive effects of elevated plasma glucose and free fatty acid levels on glucagon secretion in normal and insulin-dependent diabetic subjects. Evidence for selective alpha-cell insensitivity to glucose in diabetes mellitus.

To examine whether abnormal pancreatic alpha-cell function found in human diabetes mellitus may represent a selective insensitivity to glucose, plasma glucagon responses to hyperglycemia and elevation of plasma free fatty acid levels (both known suppressors of glucagon secretion) were compared in juvenile-onset, insulin-requiring diabetic subjects, and in normal nondiabetic subjects. In the latter, both elevation of plasma free fatty acid levels induced by heparin administration of hyperglycemia produced by intravenous infusion of glucose resulted in a comparable 30--40% suppression of circulating glucagon levels (P less than 0.01). In the diabetic subjects, glucagon suppression by hyperglycemia (less than 20%) was less than that occurring in normal subjects (P less than 0.01), even when accompanied by infusion of supraphysiologic amounts of insulin. However, suppression of glucagon levels by elevation of plasma free fatty acids in the diabetic group was similar to that found in normal subjects and of comparable magnitude to that due to hyperglycemia in the normal subjects. These results thus demonstrate a selective impairment of the diabetic alpha-cell response to glucose and provide further evidence for the presence of an abnormal alpha-cell glucoreceptor in human diabetes mellitus.

Adult↗
PubMed1974

Effects of alternations of plasma free fatty acid levels on pancreatic glucagon secretion in man.

The present investigation was undertaken to ascertain whether alterations in plasma free fatty acids (FFA) affect pancreatic glucagon secretion in man since FFA have been reported to influence pancreatic alpha cell function in other species. Elevation of plasma FFA from a mean (+/-SE) basal level of 0.478+/-0.036 mM to 0.712+/-0.055 mM after heparin administration caused plasma glucagon levels to fall approximately 50%, from a basal value of 122+/-15 pg/ml to 59+/-14 pg/ml (P < 0.001). Lowering of plasma FFA from a basal level of 0.520+/-0.046 mM to 0.252+/-0.041 mM after nicotinic acid administration raised plasma glucagon from a basal level of 113+/-18 pg/ml to 168+/-12 pg/ml (P < 0.005). Infusion of glucose elevated plasma glucose levels to the same degree that heparin raised plasma FFA levels. This resulted in suppression of plasma glucagon despite the fact that plasma FFA levels also were suppressed. Glucagon responses to arginine were diminished after elevation of plasma FFA (P < 0.01) and during infusion of glucose (P < 0.01). Diminution of plasma FFA by nicotinic acid did not augment glucagon responses to arginine. These results thus demonstrate that rather small alterations in plasma FFA within the physiologic range have a significant effect on glucagon secretion in man. Although the effects of glucose appear to predominate over those of FFA, alterations in plasma FFA may nevertheless exert an important physiologic influence over human pancreatic alpha cell function, especially in the postabsorptive state.

Adult↗
PubMed1974

Adrenergic modulation of pancreatic glucagon secretion in man.

In order to characterize the influence of the adrenergic system on pancreatic glucagon secretion in man, changes in basal glucagon secretion during infusions of pure alpha and beta adrenergic agonists and their specific antagonists were studied. During infusion of isoproterenol (3 mug/min), a beta adrenergic agonist, plasma glucagon rose from a mean (+/-SE) basal level of 104+/-10 to 171+/-15 pg/ml, P < 0.0002. Concomitant infusion of propranolol (80 mug/min), a beta adrenergic antagonist, prevented the effects of isoproterenol, although propranolol itself had no effect on basal glucagon secretion. During infusion of methoxamine (0.5 mg/min), an alpha adrenergic agonist, plasma glucagon declined from a mean basal level of 122+/-15 to 75+/-17 pg/ml, P < 0.001. Infusion of phentolamine (0.5 mg/min), an alpha adrenergic antagonist, caused a rise in plasma glucagon from a mean basal level of 118+/-16 to 175+/-21 pg/ml, P < 0.0001. Concomitant infusion of methoxamine with phentolamine caused a reversal of the effects of phentolamine. The present studies thus confirm that catecholamines affect glucagon secretion in man and demonstrate that the pancreatic alpha cell possesses both alpha and beta adrenergic receptors. Beta adrenergic stimulation augments basal glucagon secretion, while alpha adrenergic stimulation diminishes basal glucagon secretion. Furthermore, since infusion of phentolamine, an alpha adrenergic antagonist, resulted in an elevation of basal plasma glucagon levels, there appears to be an inhibitory alpha adrenergic tone governing basal glucagon secretion. The above findings suggest that catecholamines may influence glucose homeostasis in man through their effects on both pancreatic alpha and beta cell function.

Adult↗
PubMed1973

Lack of glucagon response to hypoglycemia in diabetes: evidence for an intrinsic pancreatic alpha cell defect.

Despite excessive glucagon responses to infusion of arginine, plasma glucagon did not rise in six juvenile-type diabetics during severe insulin-induced hypoglycemia, whereas glucagon in the controls rose significantly. Thus in diabetics pancreatic alpha cells are insensitive to glucose even in the presence of large amounts of circulating insulin. An intrinsic defect common to both alpha and beta pancreatic cells-failure to recognize (or respond to) plasma glucose fluctuations-may be operative in juvenile diabetes.

Adolescent↗
PubMedDate not supplied

Haptoglobin 1F allele frequency is high among indigenous populations in the state of Durango, Mexico.

We studied haptoglobin polymorphism in Mexican populations with high Indian ancestry living in isolated and urban areas in the state of Durango. Analysis with respect to the HP*1F and HP*1S allelic subtypes by isoelectric focusing showed unusually high HP*1F allele frequencies among urban (0.370) and isolated Mexican Indians (0.383). Comparison with other population studies demonstrated a geographical cline of the HP*1F allele increasing in the same direction of the HP*1 allele, while HP*1S frequency does not show racial differences.

Alleles↗
PubMedDate not supplied

[Comparative value of temperature marker and neutralization test for subtyping of herpes simplex viruses (author's transl)].

Two methods for the differentiation of herpes simplex virus (HSV)--rct and neutralization by specific antisera--have been applied to 8 prototype strains and 105 strains isolated from various clinical cases. The evaluation of the II/I index allows to choose the most specific rabbit antisera. The rct 40 degrees 3 C marker test gives comparable results for HSV grown in RK13 and human fibroblasts as well; it is in agreement with the immunological test in 48% of the cases. The delta tc values used to express the immunological typing allow to differentiate 76% of the strains (types 1 and 2). The others (24%) are equally neutralized by both specific antisera; they represent "intermediate" strains. The infection of man and animal by HSV (type 1, 2 or "intermediate") also produces heterospecific antibodies in variable amount. From clinical and immunological data rises the hypothesis that "intermediate" strains derive from HSV1 strains by antigenic variation during a persistent infection.

Animals↗