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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous hyperalimentation allows complete nutrition and anabolism in patients who cannot be fed by the oral route. However, several complications have been reported, e.g. septicaemia and hyperglycaemina. In 51 intensive-care patients receiving hyperalimentation, 18% were found to be hyperglycaemic in spite of insulin administration. Hyperglycaemia was frequently associated with stress. In 8 patients undergoing major surgery, which was chosen as a stress model, decreased insulin and increased glucagon, growth hormone and cortisone levels were observed. These findings could explain stress-induced glucose intolerance. In a further experiment, 8 intensive-care patients were given alternative intravenous feedings with either 600g of a mixture of glucose, fructose and xylitol in a ration of 1:2:1 or 600g glucose per day. During both regimens insulin administration was required in 4 patients, but the insulin dosage was lower with the mixture. Plasma glucose during glucose infusion was 205+/-25mg/100ml(M+/-SEM) and the sum of plasma glucose, fructose and xylitol during infusion of the mixture was 176+/-33mg/100ml, the difference being of borderline significance (p less than 0.05). The advantages and disadvantages of infusable substrates are summarized on the basis of the available literature and it is concluded that, in general, glucose is preferable. However, if hyperglycaemia is difficult to control, partial replacement of glucose by glucose substitutes or fat emulsions may be advantageous. A routine infusion programme for central venous feeding is suggested. Causes and prevention of side-effects are reviewed. In many patients receiving central venous nutrition less hazardous and less expensive methods could be used such as nasogastric tube feeding, elemental diet or peripheral venous nutrition.
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PMID:[Parenteral hyperalimentation (author's transl)]. 40 48

We have recently reported that the "in situ" myocardial concentrations of the active form of the Pyruvate Dehydrogenase Complex (PDHa) were significantly decreased in hearts obtained from normal rats fed for 3 weeks on an isocaloric sucrose rich (63%) diet (SRD) when compared to age matched controls fed on the standard laboratory chow (STD). Since, on the one hand SRD rats present glucose intolerance and impaired "in vivo" insulin action and, on the other hand the effects of insulin on the interconversion of heart PDH remains a controversial matter, we found it relevant to study the effects of insulin on the PDH complex in the "in vitro" perfused (Langendorff technique) heart preparations obtained from SRD rats. After a 35 minute perfusion period with 5.5 mM glucose as the only nutrient in the perfusate, PDHa as a percentage of total PDH was found to remain significantly lower in SRD hearts (M +/- SEM 32.6 +/- 2.3) when compared to STD hearts (68.3 +/- 4.6, P less than 0.05) in spite of comparable total PDH activities in both groups of animals. Although the addition of insulin to the perfusate (20 mu/ml) resulted in a significant increase in the percentage of PDHa (45.8 +/- 3.4) of SRD heart, values attained still remained significantly lower than those obtained in STD controls (67.5 +/- 3.6; P less than 0.05). Simultaneously, the addition of insulin to the perfusate, significantly reduced the Acetyl-CoA/CoASH ratio in SRD hearts although this ratio remained still much higher than those observed in STD controls under the same experimental conditions.
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PMID:"In vitro" effects of insulin on the PDH complex of the isolated perfused heart of rats fed a sucrose-rich diet. 151 85

Aging has been associated with glucose intolerance, insulin resistance, hyperinsulinemia, and diminished islet B-cell function. The relative contribution of these factors to the aging-associated changes in glucose tolerance has been difficult to discern, particularly so for B-cell function, since insulin sensitivity itself is a determinant of B-cell function and, therefore, comparisons of insulin levels and responses between old and young subjects are difficult. To reduce this effect, we compared B-cell function in 14 healthy older men (aged 61-82 yr; body mass index, 21-30 kg/m2), who were exercise trained for 6 months to improve insulin sensitivity, to that of 11 healthy young men (aged 24-31 yr; body mass index, 19-31 kg/m2), who were also trained. Insulin-glucose interactions were assessed by measuring indices of insulin sensitivity (SI) and glucose effectiveness at zero insulin (GEZI) using Bergman's minimal model. B-Cell function was assessed by determining the acute insulin responses (AIR) to glucose (AIRgluc) and arginine at 3 different glucose levels: fasting, approximately 14 mM, and greater than 28 mM (AIRmax). AIRmax provides a measure of B-cell secretory capacity, while the glucose level at which 50% of AIRmax occurs is termed PG50 and is used to estimate B-cell sensitivity to glucose. The insulin sensitivity and glucose effectiveness at zero insulin of the trained older subjects was similar to that of the trained young [SI: old, 5.1 +/- 0.6; young, 6.5 +/- 0.7 x 10(-5) min-1/pM (mean +/- SEM; P = NS); GEZI: old, 1.3 +/- 0.2; young, 1.7 +/- 0.2 x 10(-2) min (P = NS)]. Under these conditions, the fasting glucose levels (old, 5.4 +/- 0.2; young, 5.1 +/- 0.1 mM) and basal insulin levels (old, 49 +/- 6; young, 63 +/- 11 pM) were also similar in the two groups. AIRgluc values were lower in the exercised elderly (old, 253 +/- 50; young, 543 +/- 101 pM; P = 0.01). This decrease in stimulated insulin release was due solely to a reduction in the AIRmax (old, 1277 +/- 179; young, 2321 +/- 225 pM; P less than 0.005); the PG50 was not different (old, 8.9 +/- 0.4; young, 8.8 +/- 0.2 mM; P = NS). These differences in the older subjects were associated with a reduction in iv glucose tolerance (old, 1.49 +/- 0.15; young, 1.95 +/- 0.13%/min; P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Exercise training delineates the importance of B-cell dysfunction to the glucose intolerance of human aging. 159 79

In a prospective study concerning the pathogenesis of impaired glucose tolerance and Type 2 (non-insulin-dependent) diabetes mellitus, 346 subjects with no clinical history of diabetes were given a standard 75 g oral glucose tolerance test. The expected positive associations between 120-min plasma glucose concentration and age and body mass index were observed in both sexes and between 120-min plasma glucose and waist/hip ratio in male subjects. An unexpected negative correlation was found between 120-min plasma glucose and height in both sexes (r = -0.23, (95% confidence interval, -0.38 - -0.07) p less than 0.007 for male subjects and r = -0.24, (-0.37 - -0.11) p less than 0.006 for female subjects). These negative associations with height remained significant after controlling for age and body mass index in male subjects but not in female subjects. In the latter a highly significant negative relationship of height with age was recorded (r = -0.33, (-0.45 - -0.20) p less than 0.0001). Comparison between individuals with impaired glucose tolerance and control subjects matched for sex, age and body mass index showed that subjects with impaired glucose tolerance are significantly shorter. Mean (+/- SEM) height in the male subjects with impaired glucose tolerance (n = 29) was 173.4 +/- 1.1 cm vs 176.9 +/- 1.3 cm in control subjects, p = 0.02. In the female subjects (n = 39) mean (+/- SEM) height was 159.4 +/- 1.0 cm vs 162.4 +/- 1.0 cm in control subjects, p = 0.02. The negative relationship between height and glucose tolerance is a new epidemiological observation which has not been previously reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Height and glucose tolerance in adult subjects. 164 51

The 75 and 50g OGTT (Oral Glucose Tolerance Test) responses were studied in 86 normal healthy pregnant women (mean age 28.7 +/- 0.4 (SEM) years) at 28 and 32 weeks respectively. Of these were 50 Chinese, 20 Malays and 16 Indians. Mean glucose responses at fasting, 1 and 2h post glucose load were 78.3 +/- 0.7, 132.2 +/- 2.8 and 116.2 +/- 2.1 mg/dl respectively for the 75g OGTT and 78.5 +/- 0.7, 130.5 +/- 2.5 and 106.7 +/- 1.8 mg/dl respectively for the 50g OGTT. Except for the 2h responses, corresponding responses between both OGTTs were not significantly different. All races showed a similar OGTT response. Using a set criteria for diagnosis of abnormals resulted in gross inconsistency in the number of abnormals diagnosed for both OGTTs. However, the use of 95th percentile shows a closer agreement in the diagnosis of abnormal cases for both OGTTs. Also, the 2h OGTT response for the 75g OGTT is higher than that of WHO's criteria for impaired glucose tolerance. This emphasizes the need to establish our own reference range.
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PMID:The 75 and 50g OGTT response in normal pregnant women. 204 74

Fasting plasma islet amyloid polypeptide concentrations and their responses to an oral glucose load were determined in non-diabetic control subjects and patients with abnormal glucose tolerance in relation to the responses of insulin or C-peptide. Plasma islet amyloid polypeptide was measured by radioimmunoassay. In the non-diabetic control subjects, fasting plasma islet amyloid polypeptide was 6.4 +/- 0.5 fmol/ml (mean +/- SEM) and was about 1/7 less in molar basis than in insulin. The fasting islet amyloid polypeptide level rose in obese patients and fell in patients with Type 1 (insulin-dependent) diabetes mellitus. In non-obese patients with impaired glucose tolerance and Type 2 (non-insulin-dependent) diabetic patients without insulin therapy, the level was equal to that of the control subjects, but a low concentration of islet amyloid polypeptide relative to insulin or C-peptide was observed in the non-obese Type 2 diabetic group. The patterns of plasma islet amyloid polypeptide responses after oral glucose were similar to those of insulin or C-peptide. However, compared to non-obese patients, a hyper-response of islet amyloid polypeptide relative to C-peptide was noted in obese patients who had a hyper-response of insulin relative to C-peptide. This study suggests that basal hypo-secretion of islet amyloid polypeptide relative to insulin exists in non-obese Type 2 diabetes and that circulating islet amyloid polypeptide may act physiologically with insulin to modulate the glucose metabolism.
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PMID:Plasma islet amyloid polypeptide (Amylin) levels and their responses to oral glucose in type 2 (non-insulin-dependent) diabetic patients. 206 48

Glucose tolerance and insulin response were evaluated in 9 normal-weight and 6 obese cats after IV administration of 0.5 g of glucose/kg of body weight. Blood samples for glucose and insulin determinations were collected immediately prior to and 2.5, 5, 7.5, 10, 15, 30, 45, 60, 90, and 120 minutes after glucose infusion. Baseline glucose concentrations were not significantly different between normal-weight and obese cats; however, mean +/- SEM glucose tolerance was significantly impaired in obese vs normal-weight cats after glucose infusion (half time for glucose disappearance in serum--77 +/- 7 vs 51 +/- 4 minutes, P less than 0.01; glucose disappearance coefficient--0.95 +/- 0.10 vs 1.44 +/- 0.10%/min, P less than 0.01; insulinogenic index--0.20 +/- 0.02 vs 0.12 +/- 0.01, P less than 0.005, respectively). Baseline serum insulin concentrations were not significantly different between obese and normal-weight cats. Insulin peak response after glucose infusion was significantly (P less than 0.005) greater in obese than in normal-weight cats. Insulin secretion during the first 60 minutes (P less than 0.02), second 60 minutes (P less than 0.001), and total 120 minutes (P less than 0.0003) after glucose infusion was also significantly greater in obese than in normal-weight cats. Most insulin was secreted during the first hour after glucose infusion in normal-weight cats and during the second hour in obese cats. The impaired glucose tolerance and altered insulin response to glucose infusion in the obese cats was believed to be attributable to deleterious effects of obesity on insulin action and beta-cell responsiveness to stimuli (ie, glucose).
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PMID:Glucose tolerance and insulin response in normal-weight and obese cats. 220 97

Glucose tolerance and insulin secretion were studied in 56 women 6-12 years following a pregnancy complicated by gestational diabetes, and in 23 matched controls. At recall 14 women were known to have diabetes and five were again pregnant with recurrent gestational diabetes. The early development of diabetes was associated with a fasting plasma glucose greater than 6 mmol/l during pregnancy and with a high plasma glucose response to oral glucose which persisted after delivery. Obesity was predictive of non-insulin-dependent diabetes whereas those that later required insulin were not obese. At recall, seven of the remaining 37 women were found to have unrecognized diabetes, 13 had impaired glucose tolerance (IGT) and 17 were normal by WHO criteria using a 75 g oral glucose tolerance test. In these 37 women, fasting plasma glucose and the glucose response to oral glucose in pregnancy were not predictive of subsequent diabetes or impaired glucose tolerance. Obesity in pregnancy and subsequent weight gain were associated with non-insulin-dependent diabetes and impaired glucose tolerance at recall. Insulin deficiency was observed during the oral glucose tolerance test in the diabetics (the mean +/- SEM ratio insulin area:glucose area 4.1 +/- 1.3 diabetics, 10.7 +/- 1.8 controls, p less than 0.05), whereas in the group with impaired glucose tolerance insulin levels were high and in proportion to their hyperglycaemia (insulin area:glucose area 10.9 +/- 1.4 IGT, 9.4 +/- 1.4 controls). Women with normal glucose tolerance and previous gestational diabetes had significantly lower insulin responses than their controls, despite mild hyperglycaemia (insulin area:glucose area 4.0 +/- 0.7 normal glucose tolerance, 7.6 +/- 1.1 controls, p less than 0.02). Abnormalities of glucose tolerance and insulin secretion are present following a gestational diabetic pregnancy. Gestational diabetes identifies women at risk for developing diabetes and impaired glucose tolerance, both of which are risk factors for premature vascular disease.
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PMID:Abnormalities of glucose tolerance following gestational diabetes. 229 Sep 18

We compared the usefulness of three glycated serum proteins, glycated albumin (GA), glycated hemoglobin (HBA1c) and fructosamine (FA), for diabetic screening purposes. We measured these indices in 302 adults, most of whom underwent yearly physical examinations. We measured GA and HbA1c with high precision using high-performance liquid chromatography (interassay coefficients of variation 4.9 and 4.0%, respectively) and FA using commercial reagents (interassay coefficient of variation 1.65%). All the individuals underwent a 75-g oral glucose tolerance test, which revealed significant correlations between the values of the three glycated proteins and the four plasma glucose concentrations measured as well as the sum of these glucose concentrations, sigma BS (GA, r = 0.80; HbA1c, r = 0.80; FA, r = 0.65). On the basis of the test, 130 of the subjects were classified as normal (N), 123 as borderline and 49 as having diabetes mellitus (D) according to the criteria of the Japan Diabetes Society. Of the 123 borderline cases, 26 showed impaired glucose tolerance (IGT) according to the WHO criteria. The normal group values of GA, HbA1c and FA were 17.8 +/- 0.17% (mean +/- SEM), 5.02 +/- 0.03%, and 2.55 +/- 0.02 mM/l, respectively. Borderline and IGT subjects had significantly more GA and HbA1c than normal but not more FA (P less than 0.01). We divided the subjects into 10 groups on the basis of their sigma BS values; those with values higher than 671 +/- 4.7 mg/dl had significantly more GA and HbA1c than normal, while those with values higher than 1068 +/- 40.9 mg/dl (the most extreme cases) had significantly more FA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The relative value of glycated albumin, hemoglobin A1c and fructosamine when screening for diabetes mellitus. 261 42

Patients with cirrhosis of the liver (LC group, n = 12) frequently have glucose intolerance secondary to hepatic dysfunction. We compared HbA1 levels and other measures of blood sugar control in the LC group with those in healthy controls (N group, n = 43), patients with diabetes mellitus (DM group, n = 36), or patients with chronic hepatitis without evidence of cirrhosis (CH group, n = 12). HbA1 levels and the mean values of fasting plasma glucose for the past month (FPG) were as follows: LC group 6.40 +/- 0.36 (mean +/- SEM)% and 130 +/- 20 mg/dl, DM group 10.29 +/- 0.45% and 172 +/- 11 mg/dl, CH group 10.70 +/- 0.86% and 176 +/- 21 mg/dl, N group 6.52 +/- 0.11% and 83 +/- 1 mg/dl, respectively. HbA1 in the LC group was similar to that in the N group, although FPG in the former was higher (p less than 0.05). All groups showed statistically significant positive correlations between HbA1 levels and (a) FPG, (b) the daily profile of plasma glucose values, (c) the total or peak plasma glucose values during a 50 g-OGTT. The regression line in the LC group, however, was statistically different from that in DM or CH group. Thus, HbA1 in the LC group is lower than that in DM or CH in spite of equivalent glucose intolerance. Therefore, we suggest caution in the interpretation of HbA1 levels in hepatic cirrhosis.
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PMID:Hemoglobin A1 in cirrhosis of the liver. 262 33


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