Effects of exercise and lack of exercise on glucose tolerance and insulin sensitivity

1983 ◽  
Vol 55 (2) ◽  
pp. 512-517 ◽  
Author(s):  
G. W. Heath ◽  
J. R. Gavin ◽  
J. M. Hinderliter ◽  
J. M. Hagberg ◽  
S. A. Bloomfield ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Insulin Response ◽  
Insulin Binding ◽  
Normal Glucose Tolerance ◽  
Residual Effects ◽  
Oral Glucose ◽  
Glucose Load ◽  
Plasma Insulin Concentration ◽  
Normal Glucose ◽  
Blood Glucose Concentrations

Physically trained individuals have a markedly blunted insulin response to a glucose load and yet have normal glucose tolerance. This phenomenon has generally been ascribed to long-term adaptations to training which correlate with maximal oxygen uptake (VO2max) and reduced adiposity. Our study was undertaken to test the hypothesis that residual effects of the last bouts of exercise play an important role in this phenomenon. Eight well-trained subjects stopped training for 10 days. There were no significant changes in VO2max (58.6 +/- 2.2 vs. 57.6 +/- 2.1 ml/kg), estimated percent body fat (12.5 +/- 0.7 vs. 12.5 +/- 0.8%), or body weight. The maximum rise in plasma insulin concentration in response to a 100-g oral glucose load was 100% higher after 10 days without exercise than when the subjects were exercising regularly. Despite the increased insulin levels, blood glucose concentrations were higher after 10 days without exercise. Insulin binding to monocytes also decreased with physical inactivity. One bout of exercise after 11 days without exercise returned insulin binding and the insulin and glucose responses to an oral 100-g glucose load almost to the initial “trained” value. These results support our hypothesis.

Effect of hyperglycaemia on glucose concentration of human nasal secretions

2004 ◽  
Vol 106 (5) ◽  
pp. 527-533 ◽  
Author(s):  
David M. WOOD ◽  
Amanda L. BRENNAN ◽  
Barbara J. PHILIPS ◽  
Emma H. BAKER
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Normal Glucose ◽  
Nasal Secretions ◽  
Blood Glucose Concentrations ◽  
Glucose Threshold

Glucose is not detectable in airways secretions of normoglycaemic volunteers, but is present at 1–9 mmol·l-1 in airways secretions from people with hyperglycaemia. These observations suggest the existence of a blood glucose threshold at which glucose appears in airways secretions, similar to that seen in renal and salivary epithelia. In the present study we determined the blood glucose threshold at which glucose appears in nasal secretions. Blood glucose concentrations were raised in healthy human volunteers by 20% dextrose intravenous infusion or 75 g oral glucose load. Nasal glucose concentrations were measured using modified glucose oxidase sticks as blood glucose concentrations were raised. Glucose appeared rapidly in nasal secretions once blood glucose was clamped at approx. 12 mmol·l-1 (n=6). On removal of the clamp, nasal glucose fell to baseline levels in parallel with blood glucose concentrations. An airway glucose threshold of 6.7–9.7 mmol·l-1 was identified (n=12). In six subjects with normal glucose tolerance, blood glucose concentrations rose above the airways threshold and nasal glucose became detectable following an oral glucose load. The presence of an airway glucose threshold suggests that active glucose transport by airway epithelial cells normally maintains low glucose concentrations in airways secretions. Blood glucose exceeds the airway threshold after a glucose load even in people with normal glucose tolerance, so it is likely that people with diabetes or hyperglycaemia spend a significant proportion of each day with glucose in their airways secretions.

scholarly journals Insulin Response to Oral Glucose Load is Associated with Coronary Artery Disease in Subjects with Normal Glucose Tolerance

2008 ◽  
Vol 15 (1) ◽  
pp. 6-12 ◽  
Author(s):  
Tetsuro Miyazaki ◽  
Kazunori Shimada ◽  
Yoshitaka Iwama ◽  
Atsumi Kume ◽  
Katsuhiko Sumiyoshi ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Glucose Tolerance ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Normal Glucose ◽  
Artery Disease

Response of incretins (GIP and GLP-1) to an oral glucose load in female and male subjects with normal glucose tolerance

2014 ◽  
Vol 106 (2) ◽  
pp. e25-e29 ◽  
Author(s):  
Toshihiro Matsuo ◽  
Yoshiki Kusunoki ◽  
Tomoyuki Katsuno ◽  
Takashi Ikawa ◽  
Takafumi Akagami ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Normal Glucose ◽  
Male Subjects

PLASMA CORTICOSTEROID, PLASMA INSULIN AND BLOOD SUGAR OF NORMAL FASTING AND DIABETIC SUBJECTS WITH OR WITHOUT HYPERCORTICISM

1968 ◽  
Vol 58 (4) ◽  
pp. 643-654 ◽  
Author(s):  
Vivian Harding Asfeldt ◽  
Kai R. Jørgensen
Keyword(s):  
Glucose Tolerance ◽  
Blood Sugar ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Tolerance Test ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Acth Stimulation ◽  
Normal Glucose ◽  
Plasma Insulin Response

ABSTRACT Transient, maximum stimulation with β1–24 corticotrophin has been carried out in nine normal fasting subjects, in two fasting diabetics without hypercorticism and in three fasting diabetics with hypercorticism. Fluorimetric determinations of corticosteroids and determinations of immunological detectable insulin in plasma and blood sugar were made during stimulation. No significant variation in the blood sugar or the plasma insulin during transient, maximum ACTH stimulation was found either in normal fasting subjects or in fasting diabetics with or without hypercorticism. Moreover, in two diabetics with hypercorticism the plasma insulin response was measured during an oral glucose tolerance test. After treatment for approximately seven months with glucocorticosteroids, a reduced glucose tolerance and an increased plasma insulin response were found in one of these two patients. Four and a half months after the termination of steroid treatment, normal glucose tolerance and normal insulin responses were observed. In one patient, after several years of hypercorticism, a reduced glucose tolerance and a markedly reduced plasma insulin response were found.

Psychiatric Aspects of Diabetes—a Physician's View

1981 ◽  
Vol 139 (6) ◽  
pp. 485-493 ◽  
Author(s):  
R. B. Tattersall
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Common Factor ◽  
Fasting Blood Glucose ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Glucose Load ◽  
Normal Glucose

A raised blood sugar level no more defines a single entity than does a raised bilirubin or a low haemoglobin. Diabetes is a heterogenous group of disorders whose only common factor is hyperglycaemia (Tattersallet al, 1980). The classification of diabetes is being revised, although the changes are of more relevance to epidemiologists than clinicians. Previous standards of normal glucose tolerance were set too low, so that some people were labelled diabetic who had no symptoms and have proved on follow-up not to be at risk of developing complications such as retinopathy (i.e. they had a non-disease). Epidemiological evidence suggests that the cut-off point for ‘true’ diabetes (i.e. a condition which leads to complications and shortening of life span) is a blood glucose level two hours after a 50 G oral glucose load of 11.1 mMol/L (National Diabetes Data Group, 1979). This corresponds to a fasting blood glucose level of 7 mMol/L or below. Hence, a single blood glucose value, either in the fasting state or two hours after a 50 G glucose load, is enough to diagnose diabetes and glucose tolerance tests should hardly ever be necessary.

scholarly journals The Insulin Response to Oral Glucose in GIP and GLP-1 Receptor Knockout Mice: Review of the Literature and Stepwise Glucose Dose Response Studies in Female Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Bo Ahrén ◽  
Yuichiro Yamada ◽  
Yutaka Seino
Keyword(s):  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Incretin Hormones ◽  
Incretin Hormone ◽  
Impaired Insulin ◽  
Normal Glucose ◽  
Gip Receptor

A key factor for the insulin response to oral glucose is the pro-glucagon derived incretin hormone glucagon-like peptide-1 (GLP-1), together with the companion incretin hormone, glucose-dependent insulinotropic polypeptide (GIP). Studies in GIP and GLP-1 receptor knockout (KO) mice have been undertaken in several studies to examine this role of the incretin hormones. In the present study, we reviewed the literature on glucose and insulin responses to oral glucose in these mice. We found six publications with such studies reporting results of thirteen separate study arms. The results were not straightforward, since glucose intolerance in GIP or GLP-1 receptor KO mice were reported only in eight of the arms, whereas normal glucose tolerance was reported in five arms. A general potential weakness of the published study is that each of them have examined effects of only one single dose of glucose. In a previous study in mice with genetic deletion of both GLP-1 and GIP receptors we showed that these mice have impaired insulin response to oral glucose after large but not small glucose loads, suggesting that the relevance of the incretin hormones may be dependent on the glucose load. To further test this hypothesis, we have now performed a stepwise glucose administration through a gastric tube (from zero to 125mg) in model experiments in anesthetized female wildtype, GLP-1 receptor KO and GIP receptor KO mice. We show that GIP receptor KO mice exhibit glucose intolerance in the presence of impaired insulin response after 100 and 125 mg glucose, but not after lower doses of glucose. In contrast, GLP-1 receptor KO mice have normal glucose tolerance after all glucose loads, in the presence of a compensatory increase in the insulin response. Therefore, based on these results and the literature survey, we suggest that GIP and GLP-1 receptor KO mice retain normal glucose tolerance after oral glucose, except after large glucose loads in GIP receptor KO mice, and we also show an adaptive mechanism in GLP-1 receptor KO mice, which needs to be further examined.

Further support for heterogeneity of insulin response and insulin sensitivity in non-obese subjects with glucose intolerance

1983 ◽  
Vol 102 (3) ◽  
pp. 410-415 ◽  
Author(s):  
K. P. Ratzmann ◽  
S. Witt ◽  
B. Schulz
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Insulin Deficiency ◽  
Normal Glucose ◽  
Obese Subjects ◽  
Insulin Responses

Abstract. The relationship of insulin secretion and insulin sensitivity was studied in 67 age- and body weight-matched non-obese subjects, classified as having a normal glucose tolerance or glucose intolerance (50 g oral glucose load). Insulin response was studied by means of a 2 h glucose infusion. For the determination of insulin sensitivity a 1 h priming dose-constant insulin infusion technique was used. The per cent decrease of plasma glucose level at comparable steady-state insulin levels served as a measure of body sensitivity to exogenous insulin. In patients with glucose intolerance the early (ΔIRI area 0–5 min) and late (ΔIRI area 30–120 min) insulin responses to iv glucose were significantly reduced in comparison to controls. Controls and subjects with glucose intolerance showed considerable heterogeneity of insulin responses. Patients with glucose intolerance and relative insulin deficiency were not less responsive to insulin than subjects with normal glucose tolerance. There was, however, a wide variation of insulin sensitivity within the two groups. There was a weak significant inverse correlation between insulin response to glucose and insulin sensitivity for the two groups combined and for controls and subjects with glucose intolerance separately. The results demonstrate that the majority of non-obese patients with glucose intolerance and relative insulin deficiency does not exhibit a reduced responsiveness to insulin and therefore hypoinsulinaemia but not insulin resistance is the primary defect for an abnormal glucose tolerance in these group of subjects.

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