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  • 1
    Electronic Resource
    Electronic Resource
    Insulin resistance in alloxan-diabetic dogs: Evidence for reversal following insulin therapy (1983)
    Springer
    Diabetologia 25 (1983), S. 273-279 
    Details
    ISSN: 1432-0428
    Keywords: Alloxan ; diabetic dogs ; insulin resistance ; insulin therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hepatic glucose production and peripheral glucose utilization were measured basally and during infusion of insulin (25 and 40 mU·kg-1·h-1) in normal dogs and in insulin-deficient diabetic dogs, before and after a 10–14 day period of insulin treatment. Basal hepatic glucose production was significantly raised in the diabetic dogs (21.4±2.5 μmol·kg-1· min-1; p〈0.005) compared with normal dogs (11.9±2.5 μmol·kg-1·min-1) and fell by 20% in diabetic dogs following insulin treatment (17.4±3.0 μmol·kg-1·min-1). However, in all groups, hepatic glucose production suppressed equally well during the low dose insulin infusions, suggesting that the raised hepatic glucose production of diabetes is due to insulin deficiency and not hepatic insulin resistance. In addition, a marked defect of glucose utilization was found in the diabetic dogs (25±5 μmol·kg-1·min-1; p〈 0.001) compared with normal dogs (99±15 μmol·kg-1· min-1) during matched hyperinsulinaemia and hyperglycaemia. This defect of glucose utilization, as defined by euglycaemic insulin dose-response curves employing insulin infusion rates between 40–600 mU·kg-1·h-1, demonstrated a marked reduction of glucose disposal in diabetic dogs. The severity of the insulin resistance closely paralleled the degree of hyperglycaemia. In contrast, following 10–14 days of insulin treatment, an improvement of glucose disposal was seen in all diabetic dogs. It is concluded that insulin deficiency leads to (a) increased hepatic glucose production, and (b) the development of marked peripheral insulin resistance, which is reversed by insulin treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00279943
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  • 2
    Electronic Resource
    Electronic Resource
    Glucose utilization in Type 1 (insulin-dependent) diabetes: Evidence for a defect not reversible by acute elevations of insulin (1983)
    Springer
    Diabetologia 25 (1983), S. 331-335 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 diabetes ; glucose utilization ; insulin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has long been assumed that replacement of insulin in insulin-deficient diabetic patients will normalise glucose utilization. In this study, glucose utilization was measured in nine long-standing, poorly controlled diabetic patients and five control subjects, matched for age (33±3 versus 33±2 years) and ponderal index (22.9±1.3 versus 21.7±1.0). Glucose uptake was measured during steady state insulinaemia in the diabetic patients and control subjects, at euglycaemia (5.5±0.5 versus 5.4±0.3 mmol/l, respectively) and moderate hyperglycaemia (11.8±0.9 versus 10.2±0.7 mmol/l, respectively). At euglycaemia with similar free insulin levels (50±19 versus 43±9 mU/l; p〉 0.6), the diabetic patients utilized less glucose than the control subjects (27.8±4.2 versus 56.4±5.7 μmol · kg-1.min-1; · p〈 0.005). During hyperglycaemia, the diabetic patients utilized almost as much glucose as the control subjects did at euglycaemia (49.9±6.4 versus 56.4±5.7 μmol·kg-1 · min-1, respectively). In the control subjects, a 1-mmol/l rise in glucose concentration (with insulin remaining constant) resulted in a 12.3±1.3 μmol·kg-1·min-1 rise in glucose utilization. In contrast, in the diabetic patients, a 1-mmol/l rise in blood glucose resulted in a rise in glucose utilization of only 3.8±0.8 μmol · kg-1 · min-1 (p〈 0.001), in the presence of similar concentrations of plasma insulin. This defect of glucose utilization in Type1 diabetic patients could not be reversed by acutely raising insulin to 247±23 mU/l. It is concluded that poorly controlled, insulin-dependent diabetes has a marked defect in glucose utilization that cannot be corrected by short-term hyperinsulinaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00253196
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  • 3
    Electronic Resource
    Electronic Resource
    Differential effects of insulin therapy on hepatic and peripheral insulin sensitivity in Type 2 (non-insulin-dependent) diabetes (1982)
    Springer
    Diabetologia 23 (1982), S. 320-325 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 diabetes ; hepatic glucose production ; glucose utilization ; metabolic clearance rate of glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hepatic glucose production and metabolic clearance rate of glucose were measured using (3-3H) glucose at steady state, basally and during two sequential 2 h insulin (25 and 40mU · kg–1 · h–1)/glucose(2 and 3mg · kg–1 · min–1) infusion periods. Eight diabetic subjects were studied before and after 1 week of twice daily insulin therapy; six control subjects matched for age, weight and degree of obesity were also studied. In the diabetic patients, pre-treatment hepatic glucose production was 20.0 ± 2.2, 9.9 ± 2.9, and 1.4 ± 0.8 μmol · kg–1 · min–1 respectively (± SEM) for each of the three periods, and fell significantly with treatment to 12.8 ± 1.7,4.0 ± 1.5 and 1.9 ± 1.0 μmol · kg–1 · min–1. Hepatic glucose production in normal subjects was 13.2 ± 0.6, 2.2 ± 0.8 and 〈 1 μmol · kg–1 · min–1. The pre-treatment metabolic clearance rate in all diabetic studies with insulin levels ⩾ 30 mU/l was 1.10 ± 0.14 ml · kg–1 · min–1 and remained virtually unchanged following insulin therapy; this was significantly lower than in the control subjects (6.83 ± 1.02, p 〈 0.001). Basal non-esterified fatty acid levels were higher (p 〈 0.02) in the pre-treated diabetic patients compared to post-treated diabetic patients and control subjects. Non-esterified fatty acids in each group fell to similar levels during the insulin infusions, but the rate of fall was slower in the pre-treated diabetic patients. Insulin receptor binding to erythrocytes was normal in the diabetic subjects and unchanged by treatment. Therefore, following insulin treatment of uncontrolled Type 2 (non-insulin-dependent) diabetes, the initially increased basal hepatic glucose production, and decreased hepatic sensitivity, return towards normal. However, the glucose clearance remains low, despite good diabetic control, and appears to be a major factor in the continuing glucose intolerance. As insulin receptor binding is normal, the defect of glucose clearance in Type 2 diabetes appears compatible with a post-receptor defect of glucose metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00253737
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  • 4
    Electronic Resource
    Electronic Resource
    The feto-placental glucose steal phenomenon is a major cause of maternal metabolic adaptation during late pregnancy in the rat (1994)
    Springer
    Diabetologia 37 (1994), S. 976-984 
    Details
    ISSN: 1432-0428
    Keywords: Phlorizin ; glucose kinetics ; hyperinsulinaemic euglycaemic clamp ; insulin ; non-esterified fatty acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of this study was to determine the extent to which a feto-placental glucose steal phenomenon contributes to the process of maternal metabolic adaptation to late pregnancy. Glucose metabolism was studied in virgin control, pregnant rats and virgin rats with a phlorizin-induced model of the feto-placental glucose steal phenomenon. Whole body glucose kinetics and glucose uptake into individual tissues were measured in anaesthetised rats basally and during hyperinsulinaemic euglycaemic clamps. The basal glucose metabolism of the pregnant rats was closely mimicked by the phlorizin-treated rats. Basal plasma glucose was 39% and 38% lower (p〈0.0001 for both); hepatic glucose production was 21% and 26% higher (p〈0.05 for both); and plasma glucose clearance was 109% and 104% higher (p〈0.0001 for both) in the pregnant and phlorizin-treated rats, respectively, compared to the control rats. Basal glucose uptake into peripheral tissues was lower in both the pregnant and phlorizintreated compared to the control rats, being most evident in heart (p〈0.01 for both) and brown adipose tissue (p〈0.001 for both). In the clamp studies, impairment of glucose uptake into skeletal muscle was observed in both the pregnant and phlorizin-treated rats compared to the control rats. In conclusion, the feto-placental glucose steal phenomenon is a major contributing factor to postabsorptive glucose metabolism in late pregnancy. This phenomenon also contributes to the impairment of maternal insulin-stimulated peripheral glucose uptake.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400460
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  • 5
    Electronic Resource
    Electronic Resource
    The feto-placental glucose steal phenomenon is a major cause of maternal metabolic adaptation during late pregnancy in the rat (1994)
    Springer
    Diabetologia 37 (1994), S. 976-984 
    Details
    ISSN: 1432-0428
    Keywords: Key words Phlorizin ; glucose kinetics ; hyperinsulinaemic euglycaemic clamp ; insulin ; non-esterified fatty acid.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of this study was to determine the extent to which a feto-placental glucose steal phenomenon contributes to the process of maternal metabolic adaptation to late pregnancy. Glucose metabolism was studied in virgin control, pregnant rats and virgin rats with a phlorizin-induced model of the feto-placental glucose steal phenomenon. Whole body glucose kinetics and glucose uptake into individual tissues were measured in anaesthetised rats basally and during hyperinsulinaemic euglycaemic clamps. The basal glucose metabolism of the pregnant rats was closely mimicked by the phlorizin-treated rats. Basal plasma glucose was 39 % and 38 % lower (p 〈 0.0001 for both); hepatic glucose production was 21 % and 26 % higher (p 〈 0.05 for both); and plasma glucose clearance was 109 % and 104 % higher (p 〈 0.0001 for both) in the pregnant and phlorizin-treated rats, respectively, compared to the control rats. Basal glucose uptake into peripheral tissues was lower in both the pregnant and phlorizin-treated compared to the control rats, being most evident in heart (p 〈 0.01 for both) and brown adipose tissue (p 〈 0.001 for both). In the clamp studies, impairment of glucose uptake into skeletal muscle was observed in both the pregnant and phlorizin-treated rats compared to the control rats. In conclusion, the feto-placental glucose steal phenomenon is a major contributing factor to postabsorptive glucose metabolism in late pregnancy. This phenomenon also contributes to the impairment of maternal insulin-stimulated peripheral glucose uptake. [Diabetologia (1994) 37: 976–984]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400460
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  • 6
    Electronic Resource
    Electronic Resource
    Features of syndrome X develop in transgenic rats expressing a non-insulin responsive phosphoenolpyruvate carboxykinase gene (1999)
    Springer
    Diabetologia 42 (1999), S. 419-426 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin resistance ; syndrome X ; phosphoenolpyruvate carboxykinase ; glucose ; insulin ; triglycerides ; cholesterol ; obesity ; transgenic rats.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Obesity, glucose intolerance, dyslipidaemia and hypertension are a cluster of disorders (syndrome X) affecting many people. It has been hypothesised that these abnormalities are caused by insulin resistance, but definitive proof is lacking. We have developed transgenic rats in which the rate-limiting gluconeogenic enzyme, phosphoenolpyruvate carboxykinase, is non-insulin responsive. The aim of our study was to investigate whether syndrome X develops in these animals and if a high-fat diet interacts with this genetic defect. Methods. Chow-fed transgenic and control rats aged 1, 3, 6 and 17 months and a subgroup of transgenic and control rats fed chow plus cafeteria foods for 6 months were examined for features of syndrome X. Results. At 3 months, transgenic rats had fasting and postprandial hyperinsulinaemia, mild obesity (in abdominal and, to a lesser extent, peripheral regions) and fasting hypercholesterolaemia. Hypertriglyceridaemia was evident after 6 months while hyperglycaemia was apparent at 17 months. Hypertension had not developed by 17 months. The effect of a high-fat diet on insulin, glucose, body weight and body fat was more dramatic than the effect of the transgene alone while the effect of a high-fat diet on cholesterol and triglyceride was similar to the transgene. This illustrates that a high-fat diet is a potent catalyst for many abnormalities associated with syndrome X. There was no evidence of an additive effect of the high-fat diet plus transgene. Conclusion/interpretation. Therefore rats genetically-engineered with a non-insulin responsive gluconeogenic enzyme develop several aspects of syndrome X, supporting the hypothesis that insulin resistance initiates this cluster of disorders. [Diabetologia (1999) 42: 419–426]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051174
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  • 7
    Electronic Resource
    Electronic Resource
    The biochemical basis of increased hepatic glucose production in a mouse model of type 2 (non-insulin-dependent) diabetes mellitus (1995)
    Springer
    Diabetologia 38 (1995), S. 1389-1396 
    Details
    ISSN: 1432-0428
    Keywords: Gluconeogenesis ; glycerol ; alanine ; fructose ; 1,6-bisphosphatase ; pyruvate carboxylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanism of increased hepatic glucose production in obese non-insulin-dependent diabetic (NIDDM) patients is unknown. The New Zealand Obese (NZO) mouse, a polygenic model of obesity and NIDDM shows increased hepatic glucose production. To determine the mechanism of this phenomenon, we measured gluconeogenesis from U-14C-glycerol and U-14C-alanine and relevant gluconeogenic enzymes. Gluconeogenesis from glycerol (0.07±0.01 vs 0.21±0.02 Μmol · min−1 · body mass index (BMI)−1, p〈0.005) and alanine (0.57±0.07 vs 0.99±0.07 Μmol · min−1 · BMI−1, p〈0.005) was elevated in control mice NZO vs as was glycerol turnover (0.25±0.02 vs 0.63±0.09 Μmol · min−1 · BMI−1, p〈0.05). Fructose 1,6-bisphosphatase activity (44.2±1.9 vs 55.7±4.1 nmol · min−1 · mg protein−1, p〈0.05) and protein levels (6.9±1.1 vs 16.7±2.3 arbitrary units, p〈0.01) were increased in NZO mouse livers, as was the activity of pyruvate carboxylase (0.12±0.01 vs 0.17±0.02 nmol · min−1 · mg protein−1, p〈0.05). To ascertain whether elevated lipid supply is responsible for these biochemical changes in NZO mice, we fed lean control mice a 60% fat diet for 2 weeks. Fat-fed mice were hyperinsulinaemic (76.37±4.06 vs 98.00±7.07 pmol/l, p=0.05) and had elevated plasma non-esterified fatty acid levels (0.44±0.05 vs 0.59±0.03 mmol/l, p=0.05). Fructose 1,6-bisphosphatase activity (43.86±2.54 vs 52.93±3.09 nmol · min−1 · mg protein−1, p=0.05) and protein levels (33.03±0.96 vs 40.04±1.26 arbitrary units, p=0.005) and pyruvate carboxylase activity (0.10±0.003 vs 0.14±0.01 nmol · min−1 · mg protein−1, p〈0.05) were elevated in fat-fed mice. We conclude that in NZO mice increased hepatic glucose production is due to elevated lipolysis resulting from obesity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400598
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  • 8
    Electronic Resource
    Electronic Resource
    The set point for maternal glucose homeostasis is lowered during late pregnancy in the rat: the role of the islet beta-cell and liver (1996)
    Springer
    Diabetologia 39 (1996), S. 785-792 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Pregnancy ; glucose homeostasis ; hyperinsulinaemic euglycaemic clamp ; hepatic glucose production ; insulin secretion ; rat.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of this study was to determine the effects of late pregnancy on the ability of insulin to suppress maternal hepatic glucose production in the rat. Unlike in most previous studies, suppression of hepatic glucose production was measured at levels of glycaemia above the relatively hypoglycaemic basal pregnant level. Glucose kinetics were measured using steady-state tracer methodology in chronically catheterised, conscious virgin control and pregnant rats, firstly, during basal and low-dose hyperinsulinaemic euglycaemic clamp conditions and secondly, during a three-step glucose infusion protocol (glucose infusion rates of 0, 60 and 150 μmol · kg−1· min−1). During the clamps, plasma glucose levels were not different (6.1 ± 0.4 vs 6.5 ± 0.3 mmol/l, pregnant vs virgin; N. S.), but plasma insulin levels were higher in the pregnant rats (242 ± 30 vs 154 ± 18 pmol/l, pregnant vs virgin; p 〈 0.05) most probably due to stimulated endogenous insulin release in this group. Hepatic glucose production was suppressed from basal levels by 41 % in virgin and 90 % in pregnant rats. During the glucose infusion studies, at matched insulin levels (147 ± 10 vs 152 ± 14 pmol/l), but at plasma glucose levels which were much lower in the pregnant rats (5.5 ± 0.2 vs 8.4 ± 0.6 mmol/l, pregnant vs virgin; p 〈 0.0001), hepatic glucose production was shown to be suppressed by a similar degree in both groups (41 ± 5 vs 51 ± 5 % from basal, pregnant vs virgin; N. S.). Both the plasma insulin and percentage suppression of hepatic glucose production dose responses to plasma glucose were markedly shifted to the left indicating that the plasma glucose set point is lowered in pregnancy. In conclusion, suppression of hepatic glucose production by insulin is not impaired and the set point for plasma glucose homeostasis is lowered during late pregnancy in the rat. [Diabetologia (1996) 39: 785–792]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050511
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  • 9
    Electronic Resource
    Electronic Resource
    Hyperinsulinaemia and insulin insensitivity: studies in subjects with insulinoma (1985)
    Springer
    Diabetologia 28 (1985), S. 427-431 
    Details
    ISSN: 1432-0428
    Keywords: Insulinoma ; hyperinsulinaemia ; insulin sensitivity ; insulin responsiveness
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hepatic glucose turnover, peripheral insulin sensitivity and insulin receptor binding were measured in four subjects with insulinoma before and 3 months after surgical resection of the insulinoma. Basal hepatic glucose production, quantitated employing a primed constant infusion of tritiated glucose, was low pre-operatively (5.2±1·7μmol·kg−1· min−1) but returned to normal post-operatively (14.9±2.8; normal subjects 13.9±0.8 μmol·kg−1·min−1). Paired euglycaemic dose-response curves were developed for each subject. Insulin sensitivity, expressed as a right shift of the dose-response curve (ED50), was low pre- and post-operatively. However, insulin responsiveness (Vmax) remained normal (pre-operatively 13.9±2.2, post-operatively 13.8±0.8, normal subjects 16.7±0.8ml·kg−1·min−1). There was no consistent pattern in monocyte or erythrocyte receptor binding before or after surgery. These data suggest that the chronic hyperinsulinaemia causes suppression of hepatic glucose production, and a state of insulin insensitivity which appears to be due to a post-receptor defect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00280885
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  • 10
    Electronic Resource
    Electronic Resource
    Gliclazide therapy potentiates post-receptor insulin action in obese, non-insulin dependent diabetics
    Amsterdam : Elsevier
    Journal of Steroid Biochemistry 20 (1984), S. 1497 
    Details
    ISSN: 0022-4731
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0022-4731(84)90679-4
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