PSVI-9 Effects of dietary boron supplementation on growth performance, fasting and postprandial serum insulin, and glucose concentration of pigs

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 398-398
Author(s):  
Tyler B Chevalier ◽  
Merlin D Lindemann

Abstract A 49-d experiment evaluated the effects of supplemental boron (B) on growth, and serum insulin and glucose concentration of pigs. Crossbred pigs [n = 48; initial body weight (BW) 19.18 ± 0.29 kg] were randomly allotted to 1 of 4 diets based on BW and sex. Diets were corn-SBM-based, formulated to meet NRC (2012) nutrient requirement estimates, and were supplemented with 0, 25, 50, or 100 mg B/kg diet as sodium tetraborate decahydrate. On d 20 and 41, blood samples were collected. Fasting samples were collected following an overnight fast; then a postprandial sample was taken approximately 50 minutes after the pigs had 10 minutes of ad libitum access to feed. Samples were processed and serum analyzed for insulin and glucose concentration. Increasing B levels resulted in a linear decrease for overall ADG (0.87, 0.86, 0.85, and 0.82 kg, P = 0.02). On d 20, supplemental B resulted in a quadratic response on fasting serum glucose concentration (5.25, 4.80, 4.65, and 5.01, P = 0.03) and a linear decrease in postprandial serum insulin concentration (29.1, 25.5, 18.2, and 18.1 µU/mL, P = 0.02). Furthermore, there was a tendency for a linear decrease in fasting insulin:glucose ratio (0.85, 0.84, 0.42, and 0.59, P = 0.08), which became more noticeable during the postprandial state (3.96, 3.63, 2.63, and 2.73, P = 0.02). Again on d 41, there was a quadratic response on fasting serum glucose concentration (4.32, 4.07, 3.91, and 4.68, P = 0.01) with supplemental B. Results suggest that supplemental boron may impact serum insulin and glucose concentrations by reducing the amount of insulin needed to maintain glucose concentrations. However, higher levels of supplemental boron did result in suppressed growth performance. Thus, additional research is warranted to determine the optimum level of supplemental B.

Maturitas ◽  
2012 ◽  
Vol 72 (4) ◽  
pp. 373-378 ◽  
Author(s):  
Miranda L. Davies-Tuck ◽  
Yuanyuan Wang ◽  
Anita E. Wluka ◽  
Patricia A. Berry ◽  
Graham G. Giles ◽  
...  

1975 ◽  
Vol 79 (4) ◽  
pp. 709-719 ◽  
Author(s):  
C. Kühl

ABSTRACT Glucose and insulin concentrations during basal fasting conditions and after an oral challenge with glucose have been studied during early, mid and late pregnancy and also after delivery in a group of 9 normal women. No significant changes in the fasting serum glucose concentration was observed during pregnancy. In contrast the fasting serum insulin gradually increased. No changes in the mean glucose concentration curve were observed until the second half of pregnancy where the level of the curve was significantly elevated, but statistically calculated limits of normality derived from a special study of non-pregnant normal controls were not exceeded. The serum insulin response to glucose was significantly increased at all stages of gestation and in parallel the insulin-to-glucose index calculated for the total areas below the insulin and glucose concentration curves increased significantly. The fasting insulin-to-glucose index also increased and was found to be significantly correlated to the stage of gestation. The shape of the glucose and insulin curves was modified in the opposite direction by pregnancy: the peak value of glucose was delayed whereas that of insulin was advanced. The results indicate that in pregnancy a diminished 'peripheral sensitivity' to endogenous insulin apparently develops. As it can be seen both in the basal fasting state and after challenge with glucose a permanent influence of pregnancy on serum insulin secretion seems most likely. Therefore, the possible involvement of the hormones of pregnancy should first be considered as a cause of these findings. However, different factors, e. g. altered levels of pro-insulin or glucagon, might also be involved in the mechanism.


2015 ◽  
Vol 7 (2) ◽  
pp. 41-46
Author(s):  
S Sultana ◽  
Z Zeba ◽  
A Hossain ◽  
A Khaleque ◽  
R Zinnat ◽  
...  

Hyperproinsulinemia is commonly present in subjects with impaired glucose tolerance. The present study was undertaken to investigate the proinsulin level in Bangladeshi IGT subjects and to explore its association with insulin resistance. This observational study was conducted under a case-control design with IGT subjects (n=50) and controls (n=44). IGT was diagnosed following the WHO Study Group Criteria. Serum glucose was measured by glucose-oxidase method, serum lipid profile by enzymatic method and serum insulin and serum proinsulin were measured by ELISA method. Insulin secretory capacity (HOMA%B) and insulin sensitivity (HOMA%S) were calculated from fasting serum glucose and fasting serum insulin by homeostasis model assessment. The study subjects were age- and BMI- matched. Mean (±SD) age (yrs) of the control and IGT subjects were 40±6 and 40±5 respectively (p=0.853). Mean (±SD) BMI of the control and IGT subjects were 23±3 and 22±2 respectively (p=0.123). Fasting glucose was not significantly higher in IGT subjects, but serum glucose 2 hours after 75 gm glucose load was significantly higher in IGT subjects. Median (Range) value of fasting serum glucose (mmol/l) of control and IGT subjects were 5.3 (3.8-6) and 5.2 (4-12) respectively; (p=0.297). Median (Range) value of serum glucose (mmol/l) 2 hours after 75 gm glucose load of control and IGT subjects were 6.1 (3-7.8) and 7.9 (5- 21) respectively; (p=0.001). Fasting TG was significantly higher in IGT subjects and LDL-c was significantly lower in IGT subjects. Serum Total cholesterol and HDL-c were not significantly different between the IGT and control subjects. Median (Range) value of fasting serum TG (mg/dl) of control and IGT subjects were 119 (51-474) and 178 (82-540) respectively; (p=0.001). Median (Range) value of fasting serum T chol (mg/dl) of control and IGT subjects were 180 (65-272) and 186 (140-400) respectively; (p=0.191). Median (Range) value of fasting serum HDL-C (mg/dl) of control and IGT subjects were 29 (19-45) and 31 (15-78) respectively; (p=0.914). Median (Range) value of fasting serum LDL-C (mg/dl) of control and IGT subjects were 117(29-201) and 111(41- 320) respectively; (p=0.001). Fasting serum proinsulin was significantly higher in IGT subjects. Median (Range) value of fasting serum proinsulin (pmol/l) of control and IGT subjects were 9.2(1.8-156) and 17(3-51) respectively; (p=0.001). Insulin secretory capacity (HOMA%B) was higher but insulin sensitivity (HOMA%S) was significantly lower in case of IGT subjects. Median (Range) value of HOMA%B of control and IGT subjects were 97(46-498) and 164(17-300) respectively; (p=0.001). Median (Range) value of HOMA%S of control and IGT subjects were 68(19-270) and 39(15-110) respectively (p=0.001). In multiple regression analysis a significant negative association was found between fasting proinsulin and insulin sensitivity (p=0.037). The data led to the following conclusions: a) Insulin resistance is the predominant defect in Bangladeshi IGT subjects. b) Basal proinsulin level is significantly increased in IGT subjects. c) Insulin resistance is negatively associated with serum proinsulin in IGT subjects. DOI: http://dx.doi.org/10.3329/bjmb.v7i2.22411 Bangladesh J Med Biochem 2014; 7(2): 41-46


1986 ◽  
Vol 251 (6) ◽  
pp. E644-E647 ◽  
Author(s):  
L. Jansson ◽  
C. Hellerstrom

Earlier experiments with the microsphere technique suggested that a heightened serum glucose concentration consistently leads to an increase in islet blood flow (IBF). Several lines of evidence suggest that this glucose-sensitive control mechanism is located at an extrapancreatic site. The purpose of this study was to define the possible role of the central nervous system in such a mechanism. D-glucose, L-glucose, 3-O-methylglucose, or saline were therefore infused into the carotid artery, each at a dose of 1 mg X kg body wt-1 X min-1 for 3 min, and the pancreatic and islet blood flows were measured. None of these substances affected the systemic serum glucose level. The intracarotid infusion of D-glucose, however, caused a rapid increase in both the serum insulin concentration and IBF. The blood flow to the whole pancreas nevertheless remained unchanged, indicating a redistribution of flow within the gland. Carotid infusion of the other test substances or a similar amount of D-glucose given in a femoral vein did not affect these parameters. Both the increase in serum insulin concentration and the increase in IBF caused by D-glucose could be abolished by vagotomy or administration of atropine. When the systemic blood glucose concentration was increased by intraperitoneal glucose administration (2 g/kg body wt), vagotomy blocked the increase in islet blood flow but not the concomitant insulin release. These observations suggest that the glucose-induced increase in IBF is mediated by vagal cholinergic influences.


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