scholarly journals Blood glucose and serum insulin levels in children with cystic fibrosis.

1969 ◽  
Vol 44 (235) ◽  
pp. 351-355 ◽  
Author(s):  
A. D. Milner
PEDIATRICS ◽  
1975 ◽  
Vol 55 (1) ◽  
pp. 75-82
Author(s):  
Errol G. Wilmshurst ◽  
J. Stuart Soeldner ◽  
Douglas S. Holsclaw ◽  
Robert L. Kaufmann ◽  
Harry Shwachman ◽  
...  

Eight male patients with cystic fibrosis, normal nutrition, normal physical activity, relatively mild pulmonary disease, no evidence of liver disease and no family history of diabetes mellitus underwent a series of carbohydrate tolerance tests in comparison with a group of 18 normal male subjects matched for age and body weight. Compared with the normal group, the patients with cystic fibrosis had significantly impaired glucose tolerance and significantly lower serum immunoreactive insulin levels during oral and intravenous glucose tolerance tests; serum insulin levels were also significantly lower after intravenous administration of tolbutamide in the patients with cystic fibrosis, but the reduction in blood glucose concentration in each group was not significantly different. During an intravenous insulin test, the decrease in blood glucose concentration was the same for both groups, in spite of significantly lower serum insulin levels in the patients with cystic fibrosis. The percentage fall in plasma free fatty acids was at least as great in the patients with cystic fibrosis as in normals during the test procedures, while a significant decrease in plasma alpha-amino nitrogen after intravenously administered insulin was seen only in the patients with cystic fibrosis. These studies suggest that the carbohydrate intolerance of cystic fibrosis is consequent upon an impaired insulin response to glucose, but that this insulin deficiency is partly compensated for by increased peripheral tissue sensitivity to insulin.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xishuai Wang ◽  
Zhiqing Wang ◽  
Donghui Tang

AbstractWe investigated the impact of aerobic exercise (AE) on multiple organ dysfunction syndrome (MODS), aortic injury, pathoglycemia, and death during sepsis. ICR mice were randomized into four groups: Control (Con), Lipopolysaccharide (LPS), Exercise (Ex), and Exercise + LPS (Ex + LPS) groups. Mice were trained with low-intensity for 4 weeks. LPS and Ex + LPS mice received 5 mg/kg LPS intraperitoneally for induction of sepsis. Histopathological micrographs showed the organ morphology and damage. This study examined the effects of AE on LPS-induced changes in systemic inflammation, pulmonary inflammation, lung permeability, and bronchoalveolar lavage fluid (BALF) cell count, oxidative stress-related indicators in the lung, blood glucose levels, plasma lactate levels, serum insulin levels, plasma high-mobility group box 1 (HMGB1) levels, glucose transporter 1 (Glut1) and HMGB1, silent information regulator 1 (Sirt-1), and nuclear factor erythroid 2-related factor 2 (Nrf-2) mRNA expression levels in lung tissue. AE improved sepsis-associated multiple organ dysfunction syndrome (MODS), aortic injury, hypoglycemia, and death. AE prominently decreased pulmonary inflammation, pulmonary edema, and modulated redox balance during sepsis. AE prominently decreased neutrophil content in organ. AE prominently downregulated CXCL-1, CXCL-8, IL-6, TNF-α, Glu1, and HMGB1 mRNA expression but activated IL-1RN, IL-10, Sirt-1, and Nrf-2 mRNA expression in the lung during sepsis. AE decreased the serum levels of lactate and HMGB1 but increased blood glucose levels and serum insulin levels during sepsis. A 4-week AE improves sepsis-associated MODS, aortic injury, pathoglycemia, and death. AE impairs LPS-induced lactate and HMGB1 release partly because AE increases serum insulin levels and decreases the levels of Glut1. AE is a novel therapeutic strategy for sepsis targeting aerobic glycolysis.


1984 ◽  
Vol 33 (3) ◽  
pp. 467-473 ◽  
Author(s):  
Y.A. Kesäniemi ◽  
M. Koskenvuo ◽  
T.A. Miettinen

AbstractFasting blood glucose and serum immunoreactive insulin (IRI) and the responses of blood glucose and serum IRI to peroral glucose challenge were investigated in middle-aged normoglycemic male twins of 17 monozygotic (MZ) and 18 dizygotic (DZ) pairs recruited from the Finnish Twin Cohort Study. Also, the role of obesity and diet in the regulation of glucose and insulin metabolism was estimated. The fasting and 2 hr postprandial (PP) glucose showed higher pairwise correlations in MZ (r =0.78 and 0.56) than DZ (r = 0.08 and −0.05) pairs whereas fasting and PP insulin levels and the areas under the PP glucose and insulin curves were weakly and similarly correlated in MZ and DZ twins. The pairwise correlations of the 1/2 hr and 1 hr, but not the fasting and 2 hr insulin/glucose ratios, were somewhat higher in MZ (R = 0.51 and 0.53) than DZ (r = = 0.28 and 0.30) pairs. In MZ twins, the intrapair differences in the body mass index were significantly correlated with those in the fasting and 2 hr PP glucose and insulin levels and those in the fasting and 1/2 hr insulin/glucose ratios (r from 0.47 to 0.76). Also, the intrapair differences in the dietary fat calories were correlated positively, but those in the calories derived from carbohydrates negatively, with the intrapair differences in several parameters of the glucose and insulin metabolism. These data suggest that the environmental contribution to the regulation of glucose and insulin metabolism in subjects within the normoglycemic range may be quite strong. Of the environmental factors studied, obesity and dietary fat consumption seem to have powerful regulatory roles, particularly in the response of insulin to the glucose load.


2008 ◽  
Vol 115 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Zhen Huang ◽  
Leif Jansson ◽  
Åke Sjöholm

Patients with diabetes are often treated with a statin for hyperlipidaemia and an ACE (angiotensin-converting enzyme) inhibitor or angiotensin receptor antagonist for hypertension or albuminuria. These drugs may also exert beneficial metabolic effects, causing improved glucose tolerance in patients. Gender-related differences have also been observed in the clinical responsiveness to these drugs, but the mechanism behind this is unclear. In the present study, we have investigated whether these drugs and the fatty acid palmitate influence the pancreatic microcirculation, thereby having an impact on insulin secretion and glycaemia in vivo, in spontaneously diabetic male and female Goto–Kakizaki rats. In male rats, pancreatic IBF (islet blood flow) and total PBF (pancreatic blood flow) were increased significantly by pravastatin, captopril and irbesartan. Serum insulin levels were increased by pravastatin and captopril. Palmitate suppressed pancreatic IBF and increased blood glucose. In female animals, pancreatic IBF was stimulated by captopril, candesartan and irbesartan. Total PBF was increased by captopril, candesartan and irbesartan, and by pravastatin. Palmitate suppressed pancreatic IBF and serum insulin secretion. In conclusion, the present study lends support to the view that a local pancreatic RAS (renin–angiotensin system) and pravastatin may be selectively influencing the pancreatic microcirculation and therefore affecting insulin secretion and glycaemia. NEFAs (non-esterified fatty acids) impaired pancreatic IBF, suppressed insulin secretion and increased blood glucose. Substantial gender-related differences in the vascular and metabolic responses to these drugs prevail in this animal model of diabetes.


2016 ◽  
Vol 311 (4) ◽  
pp. E763-E771 ◽  
Author(s):  
David C. Woodland ◽  
Wei Liu ◽  
Jacky Leong ◽  
Mallory L. Sears ◽  
Ping Luo ◽  
...  

Short-term high-fat consumption stimulates mouse islet β-cell replication through unknown mechanisms. Resident macrophages (MΦs) are capable of secreting various factors involved in islet development and tissue remodeling. We hypothesized that a short-term high-fat diet (HFD) promotes MΦ infiltration in pancreatic islets and that MΦs serve as a regulator of β-cell replication. To test these hypotheses and dissect mechanisms involved in HFD-induced β-cell replication, adult C57BL/6J mice were fed a HFD for 7 days with or without administration of clodronate-containing liposomes, an MΦ-depleting agent. Mouse body and epididymal fat pad weights, and nonfasting blood glucose and fasting serum insulin levels were measured, and pancreatic islet β-cell replication, oxidative stress, and MΦ infiltration were examined. Short-term HFD promoted an increase in body and epididymal fat pad weight and blood glucose levels, along with an increased fasting serum insulin concentration. β-Cell replication, islet MΦ infiltration, and the percentage of inducible NO synthase positive MΦs in the islets increased significantly in mice fed the HFD. Immunofluorescence staining for 8-oxo-2′-deoxyguanosine or activated caspase-3 revealed no significant induction of DNA damage or apoptosis, respectively. In addition, no change in stromal-derived factor 1-expressing cells was found induced by HFD. Despite continuous elevation of nonfasting blood glucose and fasting serum insulin levels, depletion of MΦs through treatments of clodronate abrogated HFD-induced β-cell replication. These findings demonstrated that HFD-induced MΦ infiltration is responsible for β-cell replication. This study suggests the existence of MΦ-mediated mechanisms in β-cell replication that are independent of insulin resistance.


Author(s):  
Meilla Dwi Andrestian ◽  
Rizal Damanik ◽  
Faisal Anwar ◽  
Nancy Dewi Yuliana

The association of liver and muscle glycogen deposits with serum insulin levels, β-cells pancreas, and fasting blood glucose (FBG) of streptozotocin (STZ)-induced hyperglycemic rats receiving Torbangun leaves extract (TE) investigated. The intervention performed on 25 8-week-old Sprague-Dawley rats divided into four groups. Seven rats separated as a normal group (N), and other rats injected with streptozotocin (STZ). Confirmation of hyperglycemic was characterized by fasting blood glucose >126 mg/dl. Treatment group which is NG (hyperglycemic rats); N (normal rats); H-IM (62.5 mg/kg BW metformin); and H-IT (620 mg/kg BW TE) for 14 days. This study revealed that TE significantly decreased FBG levels, increased insulin production, and the amount of liver glycogen deposits (a=0.01). However, the intervention did not significantly increase the amount of muscle glycogen deposits. TE administration improves β-cells, increases the liver and muscle glycogen deposits. TE was shown to have antihyperglycemic activity by improving the β-cell, increasing blood serum insulin levels, decreasing blood glucose levels, and increasing the liver glycogen deposits.


2007 ◽  
Vol 40 (11) ◽  
pp. 907-912
Author(s):  
Machiko Komatsu ◽  
Maki Kusaka ◽  
Keiji Kume ◽  
Sachi Minami ◽  
Jun Minakuchi ◽  
...  

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