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  • 1
    Electronic Resource
    Electronic Resource
    Insulin resistance in Type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridaemia (1992)
    Springer
    Diabetologia 35 (1992), S. 1140-1145 
    Details
    ISSN: 1432-0428
    Keywords: Hypertriglyceridaemia ; insulin resistance ; Type 2 (non-insulin-dependent) diabetes mellitus ; glucose metabolism ; lipid metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hypertriglyceridaemia, which is frequently seen in Type 2 (non-insulin-dependent) diabetes mellitus, is associated with insulin resistance. The connection between hypertriglyceridaemia and insulin resistance is not clear, but could be due to substrate competition between glucose and lipids. To address this question we measured glucose and lipid metabolism in 39 Type 2 diabetic patients with hypertriglyceridaemia, i. e. mean fasting serum triglyceride level equal to or above 2 mmol/l (age 59±1 years, BMI 27.4±0.5 kg/m2, HbA1c8.0±0.2%, serum triglycerides 3.2±0.2 mmol/l) and 41 Type 2 diabetic patients with normotriglyceridaemia, i. e. mean fasting serum triglyceride level below 2 mmol/l (age 58±1 years, BMI 27.0±0.7 kg/m2, HbA1c7.8±0.2 %, serum triglycerides 1.4±0.1 mmol/l). Insulin sensitivity was assessed using a 340 pmol·(m2)−1· min−1 euglycaemic insulin clamp. Substrate oxidation rates were measured with indirect calorimetry and hepatic glucose production was estimated using a primed (25 μCi)-constant (0.25 μCi/min) infusion of [3-3H]-glucose. Suppression of lipid oxidation by insulin was impaired in patients with hypertriglyceridaemia vs patients with normal triglyceride levels (3.5±0.2 vs 3.0±0.2μmol·kg−1· min−1; p〈0.05). Stimulation of glucose disposal by insulin was reduced in hypertriglyceridaemic vs normotriglyceridaemic patients (27.0±1.3 vs 31.9±1.6 μmol·kg−1·min−1; p〈0.05) primarily due to impaired glucose storage (9.8±1.0 vs 14.6±1.4μmol·kg−1·min−1; p〈0.01). In contrast, insulinstimulated glucose oxidation was similar in patients with hypertriglyceridaemia and in patients with normal triglyceride concentrations (16.9±0.8 vs 17.2±0.7μmol·kg−1·min−1). Hepatic glucose production in the basal state and during the clamp did not differ between the two groups. We conclude therefore that oxidative substrate competition between glucose and lipids does not explain insulin resistance associated with hypertriglyceridaemia in Type 2 diabetes. The question remains whether the reduced nonoxidative glucose disposal observed in the patients with hypertriglyceridaemia is genetically determined or a consequence of increased lipid oxidation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401367
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  • 2
    Electronic Resource
    Electronic Resource
    Insulin resistance, hypertension and microalbuminuria in patients with Type 2 (non-insulin-dependent) diabetes mellitus (1993)
    Springer
    Diabetologia 36 (1993), S. 642-647 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; insulin resistance ; hypertension ; lipids ; microalbuminuria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We examined the impact of hypertension and microalbuminuria on insulin sensitivity in patients with Type 2 (non-insulin-dependent) diabetes mellitus using the euglycaemic insulin clamp technique in 52 Type 2 diabetic patients and in 19 healthy control subjects. Twenty-five diabetic patients had hypertension and 19 had microalbuminuria. Hypertension per se was associated with a 27% reduction in the rate of total glucose metabolism and a 40% reduction in the rate of non-oxidative glucose metabolism compared with normotensive Type 2 diabetic patients (both p〈0.001). Glucose metabolism was also impaired in normotensive microalbuminuric patients compared with normotensive normoalbuminuric patients (29.4±2.2 vs 40.5±2.8 μmol · kg lean body mass−1 · min−1; p=0.012), primarily due to a reduction in non-oxidative glucose metabolism (12.7±2.9 vs 21.1±2.6 μmol · kg lean body mass−1 ·min−1; p=0.06). In a factorial ANOVA design, however, only hypertension (p=0.008) and the combination of hypertension and microalbuminuria (p=0.030) were significantly associated with the rate of glucose metabolism. The highest triglyceride and lowest HDL cholesterol concentrations were observed in Type 2 diabetic patients with both hypertension and microalbuminuria. Of note, glucose metabolism was indistinguishable from that in control subjects in Type 2 diabetic patients without hypertension and microalbuminuria (40.5±2.8 vs 44.4±2.8 μmol · kg lean body mass−1 · min−1). We conclude that insulin resistance in Type 2 diabetes is predominantly associated with either hypertension or microalbuminuria or with both.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404074
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  • 3
    Electronic Resource
    Electronic Resource
    Peroxovanadate and insulin action in adipocytes from NIDDM patients. Evidence against a primary defect in tyrosine phosphorylation (1997)
    Springer
    Diabetologia 40 (1997), S. 1197-1203 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Peroxovanadate ; insulin ; isoprenaline ; cAMP ; lipolysis ; glucose uptake ; tyrosine phosphorylation ; NIDDM ; adipocyte ; in vitro.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied the effects of insulin and the stable peroxovanadate compound potassium bisperoxopicolinatooxovanadate (bpV(pic)), a potent inhibitor of phosphotyrosine phosphatases, on lipolysis and glucose uptake in subcutaneous adipocytes from 10 male patients with non-insulin-dependent diabetes mellitus (NIDDM) and 10 matched non-diabetic control subjects. Lipolysis stimulated by isoprenaline or the cAMP analogue, 8-bromo-cyclic AMP (8-br-cAMP), was reduced by approximately 40 % in NIDDM compared to control subjects. In both groups bpV(pic) exerted an antilipolytic effect that was similar to insulin (∼ 50 % inhibition). 14C-U-glucose uptake was dose-dependently increased by bpV(pic) treatment, but this effect and also that of insulin were impaired in NIDDM compared to control (bpV(pic) 1.6-fold vs 2.4-fold and insulin 2.2-fold vs 3.4-fold). Furthermore, low concentrations of bpV(pic) did not affect insulin-stimulated glucose uptake, although tyrosine phosphorylation of the insulin receptor β-subunit was clearly increased by bpV(pic). In conclusion, 1) β-adrenergic stimulation of lipolysis in vitro is attenuated in NIDDM adipocytes due to post-receptor mechanisms. 2) Both insulin and bpV(pic) decrease lipolysis and enhance glucose uptake in control as well as NIDDM adipocytes. The effect on glucose uptake, but not that on lipolysis, is impaired in NIDDM cells. 3) Peroxovanadate does not improve sensitivity and responsiveness to insulin in NIDDM adipocytes, showing that insulin-resistant glucose uptake in NIDDM is not overcome by phosphotyrosine-phosphatase inhibition and, thus, probably is not caused by impaired tyrosine phosphorylation events alone. [Diabetologia (1997) 40: 1197–1203]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050807
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  • 4
    Electronic Resource
    Electronic Resource
    Metabolic characteristics of autoimmune diabetes mellitus in adults (1991)
    Springer
    Diabetologia 34 (1991), S. 46-51 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes mellitus ; Type 2 (non-insulin-dependent) diabetes ; islet cell antibodies ; glucose metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is still a matter of debate whether patients who develop islet-cell antibody positive autoimmune diabetes during adulthood represent slowly evolving Type 1 (insulindependent) diabetes mellitus or a separate subgroup of Type 2 (non-insulin-dependent) diabetes. To address this question, we measured C-peptide response to a test meal, and energy metabolism in the basal state and during a euglycaemic, hyperinsulinaemic clamp in (1) 29 patients with Type 2 diabetes; (2) 10 patients with autoimmune diabetes developing after the age of 40 years; (3) 11 patients with Type 1 diabetes and (4) 15 non-diabetic control subjects. While C-peptide response to a test meal was lacking in Type 1 diabetes and nearly normal in Type 2 diabetes, the C-peptide response in autoimmune diabetes was markedly reduced. Patients with Type 2 diabetes, autoimmune diabetes and Type 1 diabetes showed a 47%, 45% and 42%, respectively, reduction in the rate of non-oxidative glucose metabolism compared with control subjects (p〈0.05-0.01). Similarly, patients with Type 2 diabetes (+52%), autoimmune diabetes (+27%) and Type 1 diabetes (+33%) presented with an enhanced basal rate of hepatic glucose production, which was less suppressed by insulin compared with healthy control subjects (p〈0.01). However, patients with autoimmune diabetes derived more energy from oxidation of glucose and proteins and less energy from oxidation of lipids than patients with either Type 1 or Type 2 diabetes (p〈0.05-0.01). In conclusion, patients who develop autoimmune diabetes during adulthood share the defects in hepatic glucose production and in non-oxidative glucose metabolism with both Type 1 and Type 2 diabetes. Oxidative energy metabolism in autoimmune diabetes, however, differs from that observed in Type 1 and Type 2 diabetes. Given the metabolic characteristics of these patients, it seems justified to consider autoimmune diabetes in adults as a subgroup of diabetes developing in adult age.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404024
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  • 5
    Electronic Resource
    Electronic Resource
    Non-esterified fatty acids do not contribute to insulin resistance in persons at increased risk of developing Type 2 (non-insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 192-197 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; insulin sensitivity ; peripheral glucose utilisation ; non-esterified fatty acids ; risk group
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanisms underlying insulin resistance in Type 2 (non-insulin-dependent) diabetes mellitus are not fully understood. An enhanced lipid/non-esterified fatty acid oxidation could provide an explanation. To test this hypothesis we examined the relationship between glucose and lipid metabolism in 44 first-degree relatives (28 glucose-tolerant and 16 glucose-intolerant) of Type 2 diabetic patients and in 18 healthy control subjects. Total body glucose disposal was impaired among both glucose-tolerant and glucose-intolerant relatives compared with control subjects (36.3±3.8 and 30.4±2.7 vs 47.7±3.4 μmol · kgLBM/s-1· min−1; p 〈 0.05). The impairment in glucose disposal among the relatives was primarily accounted for by impaired non-oxidative glucose metabolism (14.8±3.0 and 12.5±1.8 vs 25.3±3.1 μmol · kgLBM−1 · min−1; p 〈0.05). Plasma non-esterified fatty acid concentrations were similar in both glucose-tolerant and glucose-intolerant relatives and control subjects (646±36,649±43 and 615±41 μmol/l) and showed the same degree of suppression by insulin (99±8, 86±7 and 84±9 μmol/l). Basal lipid oxidation was similar in all groups (1.29±0.09, 1.52±0.13 and 1.49±0.21 μmol · kgLBM−1· min−1). Furthermore, insulin suppressed lipid oxidation to the same degree in glucose-tolerant, glucose-intolerant relatives and control subjects (0.65±0.13, 0.88±0.15 and 0.59±0.09μmol · kgLBM−1 · min−1). An inverse correlation between plasma non-esterified fatty acid concentration and total body glucose disposal was observed in the group of control subjects (r=−0.540; p〈0.05), but not among the relatives (r=0.002; p=N.S.). In conclusion the present data challenge the view that the “glucose-fatty acid cycle” contributes to the insulin resistance seen in first-degree relatives of patients with Type 2 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418275
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  • 6
    Electronic Resource
    Electronic Resource
    Islet amyloid polypeptide plasma concentrations in individuals at increased risk of developing Type 2 (non-insulin-dependent) diabetes mellitus (1992)
    Springer
    Diabetologia 35 (1992), S. 291-293 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; insulin resistance ; first-degree relatives ; islet amyloid polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To study whether abnormal secretion of islet amyloid polypeptide is involved in the development of insulin resistance and impaired insulin secretion in Type 2 (noninsulin-dependent) diabetes mellitus, we measured islet amyloid polypeptide concentrations in 56 first-degree relatives of Type 2 diabetic subjects and in 10 healthy control subjects. Fasting islet amyloid polypeptide concentrations were similar in control subjects, glucose-tolerant and glucose-intolerant relatives (8±1, 9±1 and 11±2 fmol/ml; p=NS). The area under the islet amyloid polypeptide curve measured during an oral glucose load was larger in glucose-intolerant relatives (115±13 fmol/ml) compared to glucose tolerant relatives and control subjects (88±3 and 79±12 fmol/ml; p〈0.05). The insulin response during the oral glucose load was inversely correlated with the rate of glucose disposal measured during a euglycaemic hyperinsulinaemic clamp (r=−0.725; p〈0.01), while no significant correlation was observed between the corresponding values for islet amyloid polypeptide and glucose disposal (r=−0.380; p=NS). Hypersecretion of islet amyloid polypeptide is observed in glucose-intolerant first-degree relatives of patients with Type 2 diabetes. Since these patients are characterized by insulin resistance and abnormal first-phase insulin secretion, the putative role of islet amyloid polypeptide in the development of these abnormalities remains to be established. It is however, unlikely that islet amyloid polypeptide is involved in the development of insulin resistance as insulin-resistant relatives with normal glucose-tolerance showed normal islet amyloid polypeptide concentrations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400933
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  • 7
    Electronic Resource
    Electronic Resource
    Insulin resistance and abnormal albumin excretion in non-diabetic first-degree relatives of patients with NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 363-369 
    Details
    ISSN: 1432-0428
    Keywords: Key words Microalbuminuria ; insulin resistance syndrome ; insulin sensitivity ; euglycaemic hyperinsulinaemic clamp.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microalbuminuria has recently been associated with insulin resistance in both insulin-dependent and non-insulin-dependent (NIDDM) diabetes mellitus. To establish whether microalbuminuria in non-diabetic subjects as well is associated with insulin resistance and associated abnormalities in glucose and lipid metabolism, oral glucose tolerance tests were performed with measurement of urinary albumin excretion rate, lipids and lipoproteins in 582 male non-diabetic first-degree relatives of patients with NIDDM. In addition, insulin sensitivity was assessed in 20 of these subjects with the euglycaemic hyperinsulinaemic clamp technique. Abnormal albumin excretion rate (AER), defined as AER 15–200 μg/min, was associated with higher systolic blood pressure (p 〈 0.05), higher fasting glucose values (p 〈 0.05), lower HDL-cholesterol (p 〈 0.05) and lower apolipoprotein A-I (p 〈 0.05) concentrations than observed in subjects with normal AER. The rate of glucose metabolism was lower in subjects with abnormal compared to subjects with normal albumin excretion rate (38.0 ± 2.8 vs 47.3 ± 2.4 μmol · kg lean body mass–1· min–1; p = 0.028). This difference was almost completely accounted for by a reduction in non-oxidative glucose metabolism (17.7 ± 1.9 vs 27.4 ± 2.7 μmol · kg lean body mass–1· min–1; p = 0.010), which correlated inversely with the AER (r = –0.543; p = 0.013). These results suggest that in non-diabetic individuals genetically predisposed to NIDDM, abnormal AER is associated with insulin resistance and abnormalities in glucose and lipid metabolism. [Diabetologia (1995) 38: 363 –369]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400643
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  • 8
    Electronic Resource
    Electronic Resource
    A stable peroxovanadium compound with insulin-like action in human fat cells (1996)
    Springer
    Diabetologia 39 (1996), S. 235-242 
    Details
    ISSN: 1432-0428
    Keywords: Adipocytes ; insulin ; vanadate ; peroxovanadate ; glucose uptake ; lipolysis ; tyrosine kinase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Aqueous solutions of peroxovanadium (pV) compounds are potent insulin-mimics in various types of cell. Since chemical instability is a problem with these agents, we studied the insulin-like action in human fat cells of a stable pV complex, bpV(pic). It enhanced 14C-U-glucose uptake in a dose-dependent manner by approximately twofold which was slightly less than the effect of insulin (approximately threefold). The pV complex did not alter cell-surface insulin binding and submaximal concentrations did not influence cellular sensitivity to insulin action on glucose uptake. The bpV(pic) inhibited the lipolytic effect of isoprenaline to the same extent as insulin; however, when the cGMP-inhibitable low-Km phosphodiesterase (cGI-PDE) was blocked with the specific inhibitor OPC 3911, the antilipolytic effect of insulin, but not that of bpV(pic), was completely prevented. Moreover, when lipolysis was stimulated by the non-hydrolysable cAMP analogue N6-monobutyryl cAMP, bpV(pic), in contrast to insulin, maintained an antilipolytic effect. These findings indicate that bpV(pic) exerts its antilipolytic effect not only through cGI-PDE activation, similar to the effect of insulin, but also by means of other mechanisms. The tyrosine kinase activity of insulin receptors from human placenta was not altered by the pV compound itself, whereas bpV(pic) clearly enhanced insulin-stimulated activity. In contrast, in situ tyrosine phosphorylation of the insulin receptor Β-subunit as well as that of several other proteins was clearly increased in cells which were treated with bpV(pic), whereas vanadate only amplified insulin-stimulated tyrosine phosphorylation. In conclusion, bpV(pic) exerts powerful insulin-like effects in human fat cells and may be a new and potentially useful agent in the management of insulin-resistant states.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403968
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  • 9
    Electronic Resource
    Electronic Resource
    The W64R variant of the β3-adrenergic receptor is not associated with Type II diabetes or obesity in a large Finnish sample (1999)
    Springer
    Diabetologia 42 (1999), S. 238-244 
    Details
    ISSN: 1432-0428
    Keywords: Keywordsβ3-Adrenergic receptor ; Type II diabetes ; obesity ; association.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent studies have suggested an association between Type II (non-insulin-dependent) diabetes mellitus-related phenotypes and a cytosine-to-thymidine substitution that results in the replacement of tryptophan by arginine at codon 64 (Trp64Arg or W64R) of the β 3-adrenergic receptor gene. Here, we present the results of possibly the largest association study to date on the variant in a sample of 526 families with a total of 1725 subjects, 1053 of whom had Type II diabetes. Preliminary calculations suggested that we had excellent power to detect the moderate associations which were reported in previous studies. No associations were found between the W64R variant and the following phenotypes in our sample: Type II diabetes, age at diagnosis for Type II diabetes, measures of obesity, fasting glucose, fasting insulin, minimal model variables, and systolic and diastolic blood pressures. In the analysis of plasma lipids, we detected an association between the variant and HDL ratios (HDL cholesterol/total cholesterol) (p = 0.013), which remained significant even after adjusting for sex, affection status and age. Since W64R homozygotes (n = 11) had the highest HDL ratios, however, heterozygotes had the lowest and the wild-type subjects had intermediate values, we conclude that the W64R variant is unlikely to reduce HDL ratios in a dose-dependent, pathogenic manner. [Diabetologia (1999) 42: 238–244]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051144
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  • 10
    Electronic Resource
    Electronic Resource
    Insulin sensitivity and insulin secretion in monozygotic and dizygotic twins (2000)
    Springer
    Diabetologia 43 (2000), S. 285-293 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Twins, monozygotic, dizygotic, heritability, insulin, insulin resistance.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To estimate the heritability of insulin sensitivity and insulin secretion, both of which are considered to contribute to the development of Type II (non-insulin-dependent) diabetes mellitus.¶Methods. Intraclass correlation coefficients and heritability estimates for insulin sensitivity (euglycaemic clamp) as well as first-phase and late-phase insulin secretion (intravenous glucose tolerance test) were calculated in 21 monozygotic and 20 dizygotic twin pairs of the same sex between 54 and 72 years of age.¶Results. Intrapair correlations for all traits were consistently higher in monozygotic than in dizygotic pairs. Insulin secretion correlated significantly only between monozygotic (first-phase r = 0.55; p = 0.003 and late-phase r = 0.66; p 〈 0.001) twins giving heritability estimates of 0.55 and 0.58, respectively. Insulin-stimulated glucose uptake showed a more modest correlation between monozygotic twins (r = 0.46; p = 0.015). The heritability estimate was 0.37. The heritability estimate for waist-to-hip ratio was 0.76 in female and 0.70 in male twins.¶Conclusion/interpretation. Genetic variability seems to contribute to the variance of insulin sensitivity as well as of insulin secretion. In the current study, genetic variance accounted almost 60 % for the variance in glucose-stimulated insulin secretion and almost 40 % for the variance in insulin-stimulated glucose uptake. Our data is also compatible with findings in monogenic forms of diabetes in which genetic defects in insulin secretion play a predominant part in the pathogenesis of hyperglycaemia. [Diabetologia (2000) 43: 285–293]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050046
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