RENAL MASS REDUCTION INCREASES THE RESPONSE TO EXOGENOUS INSULIN INDEPENDENT OF ACID-BASE STATUS OR PLASMA INSULIN LEVELS IN RATS.

2021 ◽  
Author(s):  
Elinor C Mannon ◽  
Christina L Sartain ◽  
Trevin C Wilkes ◽  
Jingping Sun ◽  
Aaron J Polichnowski ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Insulin Sensitivity ◽  
Renal Mass ◽  
Plasma Insulin ◽  
Exogenous Insulin ◽  
Mass Reduction ◽  
Sham Control ◽  
Acid Base ◽  
Plasma Insulin Levels ◽  
Remnant Kidney

Impairments in insulin sensitivity can occur in patients with chronic kidney disease (CKD). Correction of metabolic acidosis has been associated with improved insulin sensitivity in CKD, suggesting metabolic acidosis may directly promote insulin resistance. Despite this, the effect of acid or alkali loading on insulin sensitivity in a rodent model of CKD (remnant kidney) has not been directly investigated. Such studies could better define the relationship between blood pH and insulin sensitivity. We hypothesized that in remnant kidney rats, acid or alkali loading would promote loss of pH homeostasis and consequently decrease insulin sensitivity. To test this hypothesis, we determined the impact of alkali (2 weeks) or acid (5-7 days) loading on plasma electrolytes, acid-base balance, and insulin sensitivity in either sham control, 2/3 or 5/6 nephrectomy rats. Rats with 5/6 nephrectomy had the greatest response to insulin followed by animals with 2/3 nephrectomy and sham control rats. We found that treatment with a 0.1M sodium bicarbonate solution in drinking water had no effect on insulin sensitivity. Acid loading with 0.1M ammonium chloride resulted in significant reductions in pH and plasma bicarbonate. However, acidosis did not significantly impair insulin sensitivity. Similar effects were observed in Zucker obese rats with 5/6 nephrectomy. The effect of renal mass reduction on insulin sensitivity could not be explained by reduced insulin clearance or increased plasma insulin levels. We found that renal mass reduction alone increases sensitivity to exogenous insulin in rats, and that this is not acutely reversed by development of acidosis.

scholarly journals Aqueous extract from Mangifera indica Linn. (Anacardiaceae) leaves exerts long-term hypoglycemic effect, increases insulin sensitivity and plasma insulin levels on diabetic Wistar rats

PLoS ONE ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. e0227105
Author(s):  
Gustavo Roberto Villas Boas ◽  
João Marcos Rodrigues Lemos ◽  
Matheus William de Oliveira ◽  
Rafael Claudino dos Santos ◽  
Ana Paula Stefanello da Silveira ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Aqueous Extract ◽  
Wistar Rats ◽  
Plasma Insulin ◽  
Mangifera Indica ◽  
Hypoglycemic Effect ◽  
Insulin Levels ◽  
Plasma Insulin Levels

GLUCOSE TOLERANCE, PLASMA INSULIN LEVELS AND INSULIN SENSITIVITY IN ELDERLY PATIENTS

1979 ◽  
Vol 8 (2) ◽  
pp. 65-74 ◽  
Author(s):  
W. S. SOERJODIBROTO ◽  
C. R. C. HEARD ◽  
A. N. EXTON-SMITH
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Elderly Patients ◽  
Plasma Insulin ◽  
Insulin Levels ◽  
Plasma Insulin Levels

Enhanced renal IGF-I expression following partial kidney infarction

1993 ◽  
Vol 264 (6) ◽  
pp. F963-F967 ◽  
Author(s):  
S. A. Rogers ◽  
S. B. Miller ◽  
M. R. Hammerman
Keyword(s):  
Renal Failure ◽  
Steady State ◽  
Renal Mass ◽  
Renal Tissue ◽  
Renal Infarction ◽  
Mass Reduction ◽  
Igf I ◽  
Steady State Levels ◽  
Per Se ◽  
Remnant Kidney

Renal insulin-like growth factor (IGF)-I expression is enhanced in tissue that remains following removal of kidney mass. To characterize the expression of renal IGF-I after reduction of kidney mass by partial unilateral infarction, we measured levels of IGF-I extracted from noninfarcted (remnant) renal tissue that remained after one-half unilateral kidney infarction that was performed without (1/2NX) or with (1 1/2NX) contralateral nephrectomy. Levels of IGF-I extracted from remnant renal tissue after 1/2NX increased significantly, peaking on day 3 after renal mass reduction, and then returned toward baseline. Steady-state levels of IGF-I mRNA were also elevated on day 3, suggesting that the increase in IGF-I results from enhanced synthesis. A similar pattern of increased extracted IGF-I and elevated IGF-I mRNA occurred after 1 1/2NX. Levels of IGF-I extracted from remnant renal tissue 3 days after 1 1/2NX were not higher than levels extracted from remnant tissue 3 days after 1/2NX, and both were higher than levels of IGF-I extracted from contralateral kidneys 3 days after unilateral nephrectomy. Therefore, levels of IGF-I did not correlate with the extent of reduction of renal mass per se. We conclude that partial renal infarction provides a stimulus to enhance IGF-I expression. Increased renal IGF-I must be considered in the interpretation of findings originating from use of remnant kidney models of chronic renal failure.

scholarly journals THE EFFECTS OF EUGLVCEMIC INSULIN CLAMP ON THE METABOLISM OF 3-HYDROXVBUTYRATE AND PLASMA FREE FAHY ACIDS BY THE HIND LIMB OF LACRATING SHEEP

2021 ◽  
Vol 15 ◽  
pp. 63-69
Author(s):  
A. J. A OSUAGWUH ◽  
R. R. SMITHARD ◽  
J. METCALFE ◽  
T. E. C. WEEKES
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Hind Limb ◽  
Plasma Insulin ◽  
Extraction Ratio ◽  
Similar Relationship ◽  
Exogenous Insulin ◽  
Plasma Free Fatty Acids ◽  
Arterial Concentration ◽  
Plasma Insulin Levels

The effects of exogenous insulin, with euglycemia, on the concentration differences, extraction ratio and uptake of 3- hydroxybutyrate and plasma free fatty acids by the lactating sheep hind limb were studied. Generally, the results showed that with increasing plasma insulin levels, while maintaining euglycemia, the concentrations, arterio-venous concentration differences, extraction ratio and uptake of 3-hydrubutyrate and free fatty acids Were significantly (P<0.05) reduced, but Significant correlation was established between arterial concentration of 3-hydtoxvbutyrate and plasma free fatty acids and their uptake. A similar relationship was also obtained between the arterial concentrations of 3-hydroxybutyrate plasma free fatty acids.

Melatonin ameliorates oxidative stress, inflammation, proteinuria, and progression of renal damage in rats with renal mass reduction

2008 ◽  
Vol 294 (2) ◽  
pp. F336-F344 ◽  
Author(s):  
Yasmir Quiroz ◽  
Atilio Ferrebuz ◽  
Freddy Romero ◽  
Nosratola D. Vaziri ◽  
Bernardo Rodriguez-Iturbe
Keyword(s):  
Oxidative Stress ◽  
Renal Failure ◽  
Renal Function ◽  
Chronic Renal Failure ◽  
Renal Mass ◽  
Mass Reduction ◽  
Melatonin Treatment ◽  
Melatonin Administration ◽  
Renal Ablation ◽  
Remnant Kidney

The progressive deterioration of renal function and structure resulting from renal mass reduction are mediated by a variety of mechanisms, including oxidative stress and inflammation. Melatonin, the major product of the pineal gland, has potent_antioxidant and anti-inflammatory properties, and its production is impaired in chronic renal failure. We therefore investigated if melatonin treatment would modify the course of chronic renal failure in the remnant kidney model. We studied rats followed 12 wk after renal ablation untreated (Nx group, n = 7) and treated with melatonin administered in the drinking water (10 mg/100 ml) (Nx + MEL group, n = 8). Sham-operated rats ( n = 10) were used as controls. Melatonin administration increased 13–15 times the endogenous hormone levels. Rats in the Nx + MEL group had reduced oxidative stress (malondialdehyde levels in plasma and in the remnant kidney as well as nitrotyrosine renal abundance) and renal inflammation (p65 nuclear factor-κB-positive renal interstitial cells and infiltration of lymphocytes and macrophages). Collagen, α-smooth muscle actin, and transforming growth factor-β renal abundance were all increased in the remnant kidney of the untreated rats and were reduced significantly by melatonin treatment. Deterioration of renal function (plasma creatinine and proteinuria) and structure (glomerulosclerosis and tubulointerstitial damage) resulting from renal ablation were ameliorated significantly with melatonin treatment. In conclusion, melatonin administration improves the course of chronic renal failure in rats with renal mass reduction. Further studies are necessary to define the potential usefulness of this treatment in other animal models and in patients with chronic renal disease.

Increased renal endothelin production in rats with reduced renal mass

1991 ◽  
Vol 260 (3) ◽  
pp. F331-F339 ◽  
Author(s):  
A. Benigni ◽  
N. Perico ◽  
F. Gaspari ◽  
C. Zoja ◽  
L. Bellizzi ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Renal Mass ◽  
Excretion Rate ◽  
Mass Reduction ◽  
Cortical Tissue ◽  
Urinary Excretion Rate ◽  
Renal Cortical Tissue ◽  
Progressive Renal Disease ◽  
Remnant Kidney ◽  
Stimulation Of

Renal endothelin (ET) production was investigated in rats after renal mass ablation, a model of progressive renal disease characterized by glomerular hemodynamic alterations and capillary thrombosis, and in sham-operated animals. Thrombin stimulation of renal cortical tissue from rats with renal mass reduction, 45 but not 7 days after surgery, generated significantly (P less than 0.01) more ET than tissue from sham-operated animals. Exposure to thrombin of isolated glomeruli from remnant but not sham kidneys also significantly (P less than 0.01) increased ET production compared with unstimulated glomeruli. At day 45, in rats with renal mass ablation ET plasma levels were numerically lower, whereas urinary excretion rate of ET was significantly (P less than 0.01) increased compared with sham-operated animals. After a 50-min intravenous infusion of 125I-ET to normal rats and animals with renal mass ablation, less than 0.3% and 0.03%, respectively, of total infused radioactivity was recovered in urine. These results indicate that thrombin-stimulated ET production by renal cortical tissues is increased in rats with renal mass reduction. Despite normal or low-normal plasma ET levels, urinary excretion of the peptide is markedly increased in this model. The exogenously labeled ET added to circulation is not excreted by the kidney, suggesting that enhanced urinary excretion rate would reflect an increased renal production of the peptide in rats with remnant kidney.

scholarly journals Estrogen deprivation in primate pregnancy leads to insulin resistance in offspring

2016 ◽  
Vol 230 (2) ◽  
pp. 171-183 ◽  
Author(s):  
Adina Maniu ◽  
Graham W Aberdeen ◽  
Terrie J Lynch ◽  
Jerry L Nadler ◽  
Soon O K Kim ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Pancreatic Beta Cells ◽  
Plasma Insulin ◽  
Area Under The Curve ◽  
In Utero ◽  
Model Assessment ◽  
Insulin Levels ◽  
Plasma Insulin Levels

This study tested the hypothesis that estrogen programs mechanisms within the primate fetus that promote insulin sensitivity and glucose homeostasis in offspring. Glucose tolerance tests were performed longitudinally in prepubertal offspring of baboons untreated or treated on days 100 to 165/175 of gestation (term is 184 days) with the aromatase inhibitor letrozole, which decreased fetal estradiol levels by 95%. Basal plasma insulin levels were over two-fold greater in offspring delivered to letrozole-treated than untreated animals. Moreover, the peak 1min, average of the 1, 3, and 5min, and area under the curve blood glucose and plasma insulin levels after an i.v. bolus of glucose were greater (P<0.05 and P<0.01, respectively) in offspring deprived of estrogen in utero than in untreated animals and partially or completely restored in letrozole plus estradiol-treated baboons. The value for the homeostasis model assessment of insulin resistance was 2.5-fold greater (P<0.02) and quantitative insulin sensitivity check index lower (P<0.01) in offspring of letrozole-treated versus untreated animals and returned to almost normal in letrozole plus estradiol-treated animals. The exaggerated rise in glucose and insulin levels after glucose challenge in baboon offspring deprived of estrogen in utero indicates that pancreatic beta cells had the capacity to secrete insulin, but that peripheral glucose uptake and/or metabolism were impaired, indicative of insulin resistance and glucose intolerance. We propose that estrogen normally programs mechanisms in utero within the developing primate fetus that lead to insulin sensitivity, normal glucose tolerance, and the capacity to metabolize glucose after birth.

Effect of adrenal demedullation and (or) physical training on glucose tolerance in the rat

1993 ◽  
Vol 71 (12) ◽  
pp. 931-937 ◽  
Author(s):  
Christine Jean ◽  
Gilles Tancrède ◽  
André Nadeau
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Physical Training ◽  
Plasma Insulin ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Basal Plasma ◽  
Plasma Insulin Levels

Physical training increases insulin sensitivity by mechanisms not yet fully understood. Because exercise also modulates adrenergic system activity, the present study was designed to ascertain whether the improved glucose homeostasis observed in trained rats is influenced by epinephrine secretion from the adrenal medullae. Male Wistar rats previously submitted to adrenal demedullation or sham operated were kept sedentary or trained on a treadmill over a 10-week period. An intravenous glucose tolerance test (IVGTT) was done 64 h after the last bout of exercise. Basal plasma glucose levels were reduced by physical training (p < 0.005) and by adrenal demedullation (p < 0.001). Adrenodemedullated rats had lower (p < 0.005) plasma glucose levels than sham-operated animals over the whole glucose tolerance curve. Trained animals had lower (p < 0.01) plasma glucose levels than sedentary rats throughout the IVGTT, except at 45 min. The glucose disappearance rate measured after the glucose bolus injection was increased by training (p < 0.05), whereas it was not modified by adrenal demedullation. Basal plasma insulin levels were reduced (p < 0.001) by physical training but unaffected by adrenal demedullation. During the IVGTT, adrenodemedullated rats had higher (p < 0.01) plasma insulin levels at 2, 4, and 6 min, whereas trained animals had lower (p < 0.05) plasma insulin levels throughout the test. Moreover, insulin in adrenodemedullated and trained rats had returned to basal levels at 30 min. The area under the curve for insulin was diminished by physical training (p < 0.001) but was not modified by adrenal demedullation. In the basal state and during the IVGTT, the sedentary adrenodemedullated rats had higher (p < 0.05) plasma glucagon levels compared with the other groups of animals. Pancreatic insulin content was not modified by adrenal demedullation but was diminished (p < 0.01) by physical training. The pancreatic glucagon content was not altered by adrenal demedullation or physical training. Because adrenal demedullation abolished the exercise-induced increase in epinephrine secretion, the results of the present study suggest that the enhanced insulin sensitivity induced by physical training is not caused by an increase in epinephrine secretion from the adrenal medullae.Key words: adrenal demedullation, physical training, glucose tolerance, insulin sensitivity, catecholamines.

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