scholarly journals The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses

2017 ◽  
Vol 312 (6) ◽  
pp. R965-R972 ◽  
Author(s):  
Debra L. Irsik ◽  
Bonnie L. Blazer-Yost ◽  
Alexander Staruschenko ◽  
Michael W. Brands

Despite the effects of insulinopenia in type 1 diabetes and evidence that insulin stimulates multiple renal sodium transporters, it is not known whether normal variation in plasma insulin regulates sodium homeostasis physiologically. This study tested whether the normal postprandial increase in plasma insulin significantly attenuates renal sodium and volume losses. Rats were instrumented with chronic artery and vein catheters, housed in metabolic cages, and connected to hydraulic swivels. Measurements of urine volume and sodium excretion (UNaV) over 24 h and the 4-h postprandial period were made in control (C) rats and insulin-clamped (IC) rats in which the postprandial increase in insulin was prevented. Twenty-four-hour urine volume (36 ± 3 vs. 15 ± 2 ml/day) and UNaV (3.0 ± 0.2 vs. 2.5 ± 0.2 mmol/day) were greater in the IC compared with C rats, respectively. Four hours after rats were given a gel meal, blood glucose and urine volume were greater in IC rats, but UNaV decreased. To simulate a meal while controlling blood glucose, C and IC rats received a glucose bolus that yielded peak increases in blood glucose that were not different between groups. Urine volume (9.7 ± 0.7 vs. 6.0 ± 0.8 ml/4 h) and UNaV (0.50 ± 0.08 vs. 0.20 ± 0.06 mmol/4 h) were greater in the IC vs. C rats, respectively, over the 4-h test. These data demonstrate that the normal increase in circulating insulin in response to hyperglycemia may be required to prevent excessive renal sodium and volume losses and suggest that insulin may be a physiological regulator of sodium balance.

1985 ◽  
Vol 59 (2) ◽  
pp. 429-433 ◽  
Author(s):  
E. F. Coyle ◽  
A. R. Coggan ◽  
M. K. Hemmert ◽  
R. C. Lowe ◽  
T. J. Walters

The effect of a high-carbohydrate meal 4 h before 105 min of exercise at 70% of maximal O2 uptake was determined in seven endurance-trained cyclists and compared with exercise following a 16-h fast. The preexercise meal produced a transient elevation of plasma insulin and blood glucose, which returned to fasting basal levels prior to the initiation of exercise. The meal also resulted in a 42% elevation (P less than 0.05) of glycogen within the vastus lateralis at the beginning of exercise. The 1st h of exercise when subjects were fed was characterized by a 13–25% decline (P less than 0.05) in blood glucose concentration, a suppression of the normal increase in plasma free fatty acids and blood glycerol, and a 45% (P less than 0.05) greater rate of carbohydrate oxidation compared with exercise when subjects were fasted. After 105 min of exercise, there were no significant differences when subjects were fed or fasted regarding blood glucose levels, rate of carbohydrate oxidation, or muscle glycogen concentration. The greater muscle glycogen utilization (97 +/- 18 vs. 64 +/- 8 mmol glucosyl units X kg-1; P less than 0.05) and carbohydrate oxidation when subjects were fed appeared to be derived from the glycogen synthesized following the meal. These results indicate that preexercise feedings alter substrate availability despite a return of plasma insulin to fasting levels prior to exercise and that these effects persist until the 2nd h of exercise.


Endocrinology ◽  
2007 ◽  
Vol 148 (7) ◽  
pp. 3271-3278 ◽  
Author(s):  
Xue-Qun Chen ◽  
Jing Dong ◽  
Chen-Ying Niu ◽  
Jun-Ming Fan ◽  
Ji-Zeng Du

To determine the influence of continuous hypoxia on body weight, food intake, hepatic glycogen, circulatory glucose, insulin, glucagon, leptin, and corticosterone, and the involvement of the corticotropin-releasing factor receptor type 1 (CRFR1) in modulation of these hormones, rats were exposed to a simulated altitude of 5 km (∼10.8% O2) in a hypobaric chamber for 1, 2, 5, 10, and 15 d. Potential involvement of CRFR1 was assessed through five daily sc injections of a CRFR1 antagonist (CP-154,526) prior to hypoxia. Results showed that the levels of body weight, food intake, blood glucose, and plasma insulin were significantly reduced; the content of hepatic glycogen initially and transiently declined, whereas the early plasma glucagon and leptin remarkably increased; plasma corticosterone was markedly increased throughout the hypoxic exposure of 1–15 d. Compared with hypoxia alone, CRFR1 antagonist pretreatment in the hypoxic groups prevented the rise in corticosterone, whereas the levels of body weight and food intake were unchanged. At the same time, the reduction in blood glucose was greater and the pancreatic glucose was increased, plasma insulin reverted toward control, and plasma glucagon decreased. In summary, prolonged hypoxia reduced body weight, food intake, blood glucose, and plasma insulin but transiently enhanced plasma glucagon and leptin. In conclusion, CRFR1 is potentially involved in the plasma insulin reduction and transient glucagon increase in hypoxic rats.


1972 ◽  
Vol 70 (2) ◽  
pp. 373-384 ◽  
Author(s):  
W. N. Spellacy ◽  
W. C. Buhi ◽  
S. A. Birk

ABSTRACT Seventy-one women were treated with a daily dose of 0.25 mg of the progestogen ethynodiol diacetate. They were all tested with a three-hour oral glucose tolerance test before beginning the steroid and then again during the sixth month of use. Measurements were made of blood glucose and plasma insulin and growth hormone levels. There was a significant elevation of the blood glucose levels after steroid treatment as well as a deterioration in the tolerance curve in 12.9% of the women. The plasma insulin values were also elevated after drug treatment whereas the fasting ambulatory growth hormone levels did not significantly change. There was a significant association between the changes in glucose and insulin levels and the subject's age, control weight, or weight gain during treatment. The importance of considering the metabolic effects of the progestogen component of oral contraceptives is stressed.


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 776-P
Author(s):  
RACHEL BRANDT ◽  
MINSUN PARK ◽  
LAURIE T. QUINN ◽  
MINSEUNG CHU ◽  
YOUNGKWAN SONG ◽  
...  

MEDISAINS ◽  
2020 ◽  
Vol 18 (1) ◽  
pp. 19
Author(s):  
Fairuz Fairuz ◽  
Hasna Dewi ◽  
Humaryanto Humaryanto

Background: Therapies for hyperglycemic treatment, including insulin and oral diabetes medications, have been confirmed to cause several side effects. Thus, finding new drugs with fewer side effects is of high importance. Salung leaf herb (Psychotria malayana Jack) reported used in traditional societies as a treatment for diabetes. However, the scientific proof of this plant for diabetes treatment is still lacking.Objective: To evaluate the antidiabetic effect of the P. malayana jack in induced type 1 diabetic rats by assessing blood glucose level and pancreatic cells in white rats.Methods: Alloxan used to induce type I diabetes. Rats randomly divided into six groups. A Group P1 received 250 mg/kg BW; group P2 received 500 mg/kg BW, group P3 received 1000 mg/kg BW. While group 4 basal received no treatment, group 5 received distilled water as a negative control, and group 6 received glibenclamide as a positive control. Medications are given for six days. Glucose levels were measured, and observation of pancreatic Langerhans cell damages.Results:  A decrease in blood glucose levels observed in all treatment groups. The most significant reduction (49.76%; 1000 mg/kg BW) occurred in the P3 group. Morphological features of pancreatic Langerhans cell damage were slightly high in the P1 group.Conclusion: P. malayana Jack can consider having an antidiabetic effect in a type 1 diabetic rat by reducing blood glucose levels.


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