Prolactin as an insulin antagonist

1953 ◽  
Vol 219-219 (1-2) ◽  
Author(s):  
M.W. Sinkoff ◽  
R.C. Bodo
Keyword(s):  
Insulin Antagonist

CIRCULATING INSULIN ANTAGONISTS IN DIABETES MELLITUS: UNTREATED DIABETICS, DIABETICS DURING INFECTIONS AND ACROMEGALICS WITH DIABETES

1959 ◽  
Vol 19 (2) ◽  
pp. 174-181 ◽  
Author(s):  
J. B. FIELD ◽  
BARBARA RIGBY
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Diabetic Patient ◽  
Assay System ◽  
Onset Type ◽  
Insulin Antagonist ◽  
Insulin Inhibitor ◽  
Isolated Rat

SUMMARY Using the effect of insulin on isolated rat hemidiaphragm as an assay system, it has been possible to demonstrate a circulating insulin antagonist in some new cases of diabetes of the growth-onset type as well as during the exacerbation of diabetes secondary to infections. Three out of four acromegalics with diabetes also showed evidence of insulin antagonist, while one diabetic patient with thyrotoxicosis requiring 155 u. insulin/day had no antagonist. The antagonist present in the new diabetics and during infection exhibited some characteristics similar to the antagonist previously described during diabetic acidosis [Field & Stetten, 1956a], but different from the insulin inhibitor present during chronic insulin resistance.

scholarly journals Possible interactions between angiotensin II and insulin: effects on glucose and lipid metabolism in vivo and in vitro

2000 ◽  
Vol 167 (3) ◽  
pp. 525-531 ◽  
Author(s):  
D Patiag ◽  
X Qu ◽  
S Gray ◽  
I Idris ◽  
M Wilkes ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Insulin Sensitivity ◽  
Insulin Resistant ◽  
Receptor Mrna ◽  
Glucose And Lipid Metabolism ◽  
Sd Rats ◽  
Insulin Antagonist ◽  
Antagonist Effect

Angiotensin II (ANGII) increases insulin sensitivity in diabetic and non-diabetic subjects, even at subpressor doses, and because there is 'crosstalk' between ANGII and insulin-signaling pathways the underlying mechanism may not be due solely to changes in regional blood flow. A series of experimental studies was undertaken to evaluate the effects of ANGII on glucose and lipid metabolism in vivo and in vitro. Groups of fructose-fed, insulin-resistant Sprague-Dawley (SD) rats were pre-treated with 0.3 mg/kg per day of the AT(1)-receptor antagonist L-158 809 (n=16), or vehicle (n=16), by oral gavage. This was prior to an oral glucose tolerance test (day 5) and measurement of the effects of ANGII infusion (20 ng/kg per min i.v. for 3 h) on whole-body insulin sensitivity using the insulin suppression test (day 7). The effect of ANGII infusion on total triglyceride secretion rate (TGSR) was evaluated in normal SD rats pretreated for 7 days with L-158 809 (n=12) or vehicle (n=12). AT(1)- and AT(2)- receptor mRNA expression and [(3)H]2-deoxyglucose uptake were assessed in cultured L6 myoblasts. Short-term treatment with L-158 809 had no effect on glucose tolerance or fasting triglyceride levels in fructose-fed rats. ANGII infusion had no effect on insulin sensitivity in fructose-fed rats pretreated with vehicle (steady-state plasma glucose (SSPG) values 8.1+/-1.6 vs 8. 4+/-0.4 mmol/l), but pretreatment with L-158 809 resulted in ANGII having a modest insulin antagonist effect in this insulin-resistant model (SSPG values 9.6+/-0.3 vs 7.1+/-0.6, P<0.03). ANGII infusion had no significant effect on TGSR (e.g. 24.6+/-1.4 vs 28.4+/-0.9 mg/100 g per h in vehicle-treated animals). RT-PCR analysis showed that L6 cells express both AT(1)- and AT(2)-receptor mRNA. Incubation with ANGII (10(-9) and 10(-8) M) had no significant effect on the dose-response curve for insulin-stimulated [(3)H]2-deoxyglucose uptake. For example, C(I200) values (dose of insulin required to increase glucose uptake by 200%) were 4.5 x 10(-9) M (control) vs 3.9 x 10(-9) M and 6.2 x 10(-9) M, whereas the positive control (glucagon-like peptide-1) increased insulin sensitivity. Thus, ANGII infusion may have a modest insulin antagonist effect on glucose disposal in insulin-resistant fructose-fed rats pretreated with an AT(1)-blocker, but ANGII has no effect on TGSR or in vitro glucose uptake in L6 myoblasts. These findings are relevant to recent clinical discussions about the metabolic effects of ANGII and renin-angiotensin system blockade.

IN-VIVO EFFECTS OF THE SYNALBUMIN INSULIN ANTAGONIST AND OF B-CHAIN ALBUMIN

The Lancet ◽  
1967 ◽  
Vol 290 (7505) ◽  
pp. 21-22 ◽  
Author(s):  
Jak Jervell ◽  
John Vallance-Owen
Keyword(s):  
Insulin Antagonist ◽  
In Vivo Effects

scholarly journals The apparent effect of melatonin on glucose homeostasis in the liver

1988 ◽  
Vol 7 (2) ◽  
pp. 85-86
Author(s):  
F. A. Müller
Keyword(s):  
Glucose Homeostasis ◽  
Glucose Concentration ◽  
Incubation Medium ◽  
Liver Tissue ◽  
Apparent Effect ◽  
Insulin Antagonist

The addition of insulin to incubated liver slides gives rise to a decrease in the glucose concentration of the incubation medium. Should melatonin be added simultaneously, the effect of the insulin alone would be almost totally neutralised. The addition of glucagon to incubated liver slides has no effect on the glucose concentration of the incubation medium. Should melatonin be added simultaneously, the glucose concentration would rise considerably. It would appear that melatonin in liver tissue serves as an insulin antagonist/glucagon synergist.

THE NATURE OF THE INSULIN-ANTAGONIST ASSOCIATED WITH PLASMA-ALBUMIN

The Lancet ◽  
1958 ◽  
Vol 272 (7048) ◽  
pp. 696 ◽  
Author(s):  
J. Vallance-Owen ◽  
Elizabeth Dennes ◽  
P.N. Campbell
Keyword(s):  
Plasma Albumin ◽  
Insulin Antagonist

scholarly journals Further Characterization of an Insulin Antagonist in the Serum of Patients in Diabetic Acidosis

1957 ◽  
Vol 36 (11) ◽  
pp. 1588-1593 ◽  
Author(s):  
James B. Field ◽  
Frank Tietze ◽  
Dewitt Stetten
Keyword(s):  
Insulin Antagonist
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