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  • 1
    Electronic Resource
    Electronic Resource
    Rapid regulation of plasma membrane insulin receptors (1980)
    Springer
    Diabetologia 19 (1980), S. 211-215 
    Details
    ISSN: 1432-0428
    Keywords: Insulin ; receptor ; liver ; diabetic ; glucagon ; plasma membranes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Injection IP of insulin at a dosage of 1 μg/g body weight into normal rats produced a rapid rise in serum insulin levels from 〈 1 to 298 ng/ml, and a rapid decrease in specific 125I-insulin binding to its receptors in purified liver plasma membranes. A fall in binding was seen as early as 10 minutes after injection and binding remained decreased for up to 60 min. At 10 min, 125I-insulin binding had fallen to 59% of controls; in contrast, 125I-glucagon binding remained unchanged. Extraction of these plasma membranes followed by radioimmunoassay for insulin did not reveal appreciable amounts of exogenous insulin. The 125I-insulin dissociation rate from plasma membranes of control and insulin treated rats was the same, also indicating a lack of exogenous insulin. Scatchard analyses indicated that the decreased binding seen after insulin injection was due primarily to a change in the number of insulin receptors and not their affinity. These studies suggest, therefore, that high doses of insulin in vivo can rapidly regulate the number of plasma membrane insulin receptors in liver.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00275271
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of metformin on insulin binding to receptors in cultured human lymphocytes and cancer cells (1982)
    Springer
    Diabetologia 23 (1982), S. 131-135 
    Details
    ISSN: 1432-0428
    Keywords: Metformin ; phenformin ; biguanides ; insulin ; insulin receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of the biguanide metformin (dimethylbiguanide) on insulin binding in vitro to IM-9 lymphocytes and MCF-7 human breast cancer cells was studied. Metformin significantly increased insulin binding to both cell types: maximum increment was 47.1±7.0% 〉 control in IM-9 and 38.0±6.1% in MCF-7 cells. The dose-response curves indicated that the latter cell line was more sensitive to metformin, with a significant effect apparent at a metformin concentration of 7.7×10-6 mol/l, similar to the levels reached in patients treated with this drug. When compared with phenformin, metformin was less active in increasing insulin binding to cultured cells, the ratio between the two drug responses being similar to that of their therapeutic dosage in patients. Insulin binding increment due to metformin was reversible, was not dependent on new protein synthesis and was evident also in IM-9 lymphocytes that had been down-regulated by pre-incubation with insulin (10-7 mol/l). This effect of metformin on insulin binding to receptors may contribute to the hypoglycaemic effect of this agent in patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01271174
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  • 3
    Electronic Resource
    Electronic Resource
    Glucose regulates both glucose transport and the glucose transporter gene expression in a hamster-derived pancreatic Beta-cell line (HIT) (1991)
    Springer
    Diabetologia 34 (1991), S. 366-369 
    Details
    ISSN: 1432-0428
    Keywords: Glucose transport ; glucose transporters ; insulin secretion ; pancreatic Beta cells ; chronic high glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied the effect of chronic exposure to high glucose on the glucose transport regulation in hamster pancreatic Beta cells in permanent culture (HIT). Cells were exposed to either 5.5 mmol/l or 16.7 mmol/l glucose for 48 h and then glucose transport was studied by measuring the (3H)-2-deoxyglucose uptake for 5 and 10 min at 37 °C. The 2- deoxyglucose uptake was lower in cells pre-exposed to glucose 16.7 mmol/l for 48 h compared to cells pre-exposed to glucose 5.5 (12.0±1.6 vs 19.1±1.2 nmol/0.1 mg after 5 min, and 22.2±2.6 vs 39.0±2.9 after 10 min respectively, mean ±SEM, n=5, p 〈 0.01). In order to investigate the mechanism(s) for glucose impairment of glucose transport, we studied the glucose carrier gene expression in the same cells by Northern and slot-blot analysis. When total RNA was extracted from HIT cells cultured at either 5.5 or 16.7 mmol/l glucose and then hybridized to 32P-labelled cDNA probes for the glucose transporter 1, the glucose transporter 2 and β-actin, a significant reduction of both glucose transporter 1 (−63.9±4.1%, mean±SEM, n=3) and glucose transporter 2 (−48.9±3.2%) mRNA was observed in HIT cells cultured with high glucose. In the same experiments no change of β-actin mRNA was observed, suggesting that the effect of high glucose was specific on the glucose-transporter mRNAs. In HIT cells cultured at glucose 16.7 mmol/l the glucose-induced insulin release was also reduced compared to cells cultured at glucose 5.5 (715±19 μU · h−1 · mg−1 vs 1301±28 μU · h−1 · mg−1, respectively, mean ±SEM, n=3, p 〈 0.05). In conclusion, in hamster pancreatic Beta-cells, chronic exposure to high glucose concentrations impairs glucose transporter mRNA levels, glucose transport, and glucose-induced insulin secretion in a co-ordinate manner.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00405011
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  • 4
    Electronic Resource
    Electronic Resource
    Interleukin-1β inhibition of insulin release in rat pancreatic islets: possible involvement of G-proteins in the signal transduction pathway (1995)
    Springer
    Diabetologia 38 (1995), S. 779-784 
    Details
    ISSN: 1432-0428
    Keywords: Key words Interleukin-1β ; pertussis toxin ; cholera toxin ; pancreatic islets ; insulin secretion ; G-proteins ; nitric oxide.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In vitro exposure of rat pancreatic beta cells to interleukin-1β (IL-1β) inhibits glucose-stimulated insulin release (2140 ± 239 and 323 ± 80 pg · islet–1· h–1 at glucose levels of 16.7 mmol/l in control and IL-1β-exposed islets, respectively, n = 7, p 〈 0.001). Cholera toxin (2 μg/ml) or pertussis toxin (0.5 μg/ml) potentiated, as expected, glucose-induced insulin release in control islets, but, in addition, when added together with IL-1β, were able to prevent the IL-1β mediated inhibition of glucose-stimulated insulin secretion (2087 ± 301 and 1662 ± 173 pg · islet–1· h–1, respectively, p 〈 0.05 vs islets exposed to IL-1β alone). To investigate the mechanism by which the toxins prevent the IL-1β effect, we then measured nitrite levels, glucose oxidation and Ca2 + uptake. Nitrite levels in the culture medium were 4.2± 1.4 and 24.0 ± 5 pmol · islet–1· 24 h–1 in control islets and in IL-1β-exposed islets, respectively (n = 6, p = 0.05). In islets exposed to IL-1β and cholera or pertussis toxins, nitrite levels were 9.1 ± 3 and 12.4 ± 6 pmol · islet–1· 24 h–1, respectively (n = 6, NS vs control islets). Glucose oxidation at 16.7 mmol/l glucose was 31.1 ± 2.9 pmol · islet–1· 120 min–1 in control islets and 16.8 ± 2.7 pmol · islet–1· 120 min–1 in IL-1β-treated islets (p 〈 0.05). The addition of cholera or pertussis toxins simultaneously to IL-1β prevented the inhibition of glucose oxidation at 16.7 mmol/l glucose (32.9 ± 3.8 and 31.7 ± 3.3 pmol · islet–1· 120 min–1 in the presence of cholera or pertussis toxins, respectively). Glucose-stimulated 45Ca2 + up-take was also significantly inhibited in IL-1β-treat-ed islets when compared to control islets (7.1 ± 0.9 and 16.8 ± 3.2 pmol · islet–1· 20 min–1, respectively, p 〈 0.05). This inhibition was prevented by the presence of cholera or pertussis toxins (14.0 ± 3.8 and 11.2 ± 2.7 pmol · islet–1· 20 min–1, respectively). In conclusion, our data show that cholera and, to a lesser extent, pertussis toxins are able to partially prevent the IL-1β-induced increase in nitrite levels and block the inhibitory effects of IL-1β on different steps leading to glucose-induced insulin secretion. These findings support the possibility that in pancreatic beta cells, G-proteins may be involved or interfere with the cytokine signal transduction. [Diabetologia (1995) 38: 779–784]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050352
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  • 5
    Electronic Resource
    Electronic Resource
    Different effects of glucose and glyburide on insulin secretion in rat pancreatic islets pre-exposed to interleukin-1β. Possible involvement of K+ and Ca2+ channels (1993)
    Springer
    Diabetologia 36 (1993), S. 791-796 
    Details
    ISSN: 1432-0428
    Keywords: Interleukin-1β ; islets ; insulin secretion ; ion channels ; glyburide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In vitro islet exposure to interleukin 1β inhibits the beta-cell response to glucose. We have studied whether a similar inhibition also occurs in response to the sulphonylurea glyburide. Rat pancreatic islets were cultured for 24 h in the presence or absence of 50 U/ml interleukin 1β and then stimulated with either glucose or glyburide for 1 h at 37 °C. In control islets basal insulin secretion was 117±32 pg · islet−1 · h−1 (mean ± SEM, n=7) and greatly increased in response to 16.7 mmol/l glucose (2140±293) or 10 μmol/l glyburide (1464±234). When islets were pre-exposed to interleukin 1β, insulin release was significantly reduced in response to glucose (323±80, p〈0.001) but not in response to glyburide (1316±185). Since both glucose and glyburide influence beta-cell K+ and Ca2+ efflux, to further investigate this different response in islets exposed to interleukin 1β we measured both Rb+ efflux (as index of the ATP-sensitive K+ channel activity) and Ca2+ uptake. In control islets, the increased insulin secretion in response to 16.7 mmol/l glucose or 10 μmol/l glyburide was associated with a reduction of 86Rb efflux (decrement of −50±1.2 % and −49±2.3 %, respectively, mean ± SEM, n=5). In contrast, in interleukin 1βpre-exposed islets both glucose and glyburide stimulation only slightly modified 86Rb efflux (decrement of −19±1.9% and −5.3±3.1 %, respectively, n=5, p〈0.001). 45Ca2+ uptake in control islets was 2.6±0.4 pmol · islet−1 · 20 min−1 under basal conditions (at 2.8 mmol/l glucose), and increased to 16.8±3.2 and 10.7±2.1 pmol · islet−1 · 20 min−1 in islets stimulated with 16.7 mmol/l glucose or 10 μmol/l glyburide, respectively (mean ± SEM, n=6). 45Ca2+ uptake in interleukin 1β treated islets was higher than in control islets under basal conditions (4.6±0.6 pmol · islet−1 · 20 min−1 at 2.8 mmol/l glucose, p〈0.05), but was significantly reduced in response to glucose 16.7 mmol/l (7.1±1.1, p〈0.01 with respect to control islets). In contrast to glucose, 10 μmol/l glyburide was able to stimulate calcium uptake in interleukin 1β treated islets in a similar way to control islets (12.8±2.5). The present data demonstrate that rat pancreatic islets treated with interleukin 1β for 24 h lose their responsivity to glucose, but not to glyburide. The difference between the two secretagogues is associated with the persistent ability of glyburide to influence Ca2+ uptake even in islets with impaired K+-channel function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400351
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  • 6
    Electronic Resource
    Electronic Resource
    Copper addition prevents the inhibitory effects of interleukin 1-β on rat pancreatic islets (1995)
    Springer
    Diabetologia 38 (1995), S. 39-45 
    Details
    ISSN: 1432-0428
    Keywords: Copper ; interleukin-1β ; islets ; insulin secretion ; glucose metabolism ; nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since copper [Cu(II)] is a necessary cofactor for both intra-mitochondrial enzymes involved in energy production and hydroxyl scavenger enzymes, two hypothesised mechanisms for action of interleukin-Iβ (IL-1β), we studied whether CU(II) addition could prevent the inhibitory effect of IL-1β on insulin release and glucose oxidation in rat pancreatic islets. Islets were incubated with or without 50 U/ml IL-1β, in the presence or absence of various concentrations of Cu(II)-GHL (Cu(II) complexed with glycyl-l-histidyl-l-lysine, a tripeptide known to enhance copper uptake into cultured cells). CuSO4 (1–1000 ng/ml) was used as a control for Cu(II) effect when present as an inorganic salt. At the end of the incubation period, insulin secretion was evaluated in the presence of either 2.8 mmol/l (basal insulin secretion) or 16.7 mmol/l glucose (glucose-induced release). In control islets basal insulin secretion was 92.0±11.4 pg · islet−1 h−1 (mean ± SEM,n=7) and glucose-induced release was 2824.0±249.0 pg · islet−1 h−1. In islets pre-exposed to 50 U/ml IL-1β, basal insulin release was not significantly affected but glucose-induced insulin release was greatly reduced (841.2±76.9,n=7,p〈0.005). In islets incubated with IL-1β and Cu-GHL (0.4 μmol/l, maximal effect) basal secretion was 119.0±13.1 pg · islet−1 h−1 and glucose-induced release was 2797.2±242.2, (n=7,p〈0.01 in respect to islets exposed to IL-1β alone). In contrast to data obtained with Cu(II)-GHL, increasing concentrations of CuSO4 (up to 10 μmol/l) did not influence the inhibitory effect of IL-1β on glucose-stimulated insulin release. Glucose oxidation (in the presence of 16.7 mmol/l glucose) was 31.5±2.4 pmol · islet−1·90min−1 in control islets and 7.0±0.9 (p〈0.01) in IL-1β-exposed islets. In islets exposed to IL-1β and Cu-GHL glucose oxidation was similar to control islets (31.9±1.9). In contrast, Cu-GHL did not prevent the IL-1β-induced increase in nitric oxide production. Nitrite levels were 5±1.7, 26±5 and to 29±4 pmol · islet−1·48 h−1 (mean ± SEM,n=5) in the culture medium from control IL-1β and IL-1β+Cu-GHL exposed islets, respectively. These data indicate that the Cu(II) complexed to GHL is able to prevent the inhibitory effects of IL-1β on insulin secretion and glucose oxidation, but not on NO production. The mechanism of action of Cu-GHL is still unclear, but it might restore the activity of the enzymatic systems inhibited by IL-1β. [Diabetologia (1995) 38∶39–45]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02369351
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  • 7
    Electronic Resource
    Electronic Resource
    Inhibition of the high-affinity glucose transporter GLUT 1 affects the sensitivity to glucose in a hamster-derived pancreatic beta cell line (HIT) (1993)
    Springer
    Diabetologia 36 (1993), S. 1204-1207 
    Details
    ISSN: 1432-0428
    Keywords: GLUT 1 ; GLUT 2 ; glucokinase ; glucose sensitivity ; insulin release ; HIT cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary HIT is a hamster-derived beta-cell line which in contrast to normal beta cells that only express the high Km GLUT-2 glucose transporter, also expresses the low Km glucose transporter GLUT 1. In HIT cells the abnormal glucose transport mechanism is associated with a marked shift to the left of the glucose-induced insulin release dose-response curve. We have used this cell model to investigate whether changes in glucose transport affect the glucose-induced insulin release. HIT cells were first incubated with a concentration of cytochalasin B (0.4 μmol/l) that selectively inhibits the GLUT-1 but not the GLUT-2 transporter. The consequences of blocking glucose phosphorylation and insulin release were studied. Exposure to 0.4 μmol/l cytochalasin B for 1 h caused a selective loss of the low Km transport: the calculated Vmax of GLUT 1 was reduced from 1726±98 to 184±14 pmol · mg protein−1 5 min−1 (mean±SEM, n=6, p〈0.005), while no major difference in the high Km (GLUT-2) transport was observed. In cytochalasin B exposed HIT cells the glucose phosphorylating activity (due to hexokinase and glucokinase) was unaffected. In these cells, however, the dose-response curve of glucose-induced insulin release was significantly shifted to the right: the 50% of maximal response (increment over baseline) was reached at an average glucose concentration of 2.9±0.2 mmol/l (vs 0.6±0.01 mmol/l in control HIT cells mean±SE, n=5, p〈0.05) and the maximal effect was reached at 11.0 mmol/l glucose (vs 2.8 mmol/l in control HIT cells p〈0.005). These results are consistent with the hypothesis that the affinity of the glucose transport system may contribute to determination of the glucose threshold concentration that triggers insulin secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401067
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  • 8
    Electronic Resource
    Electronic Resource
    Copper addition prevents the inhibitory effects of interleukin 1-b on rat pancreatic islets (1995)
    Springer
    Diabetologia 38 (1995), S. 39-45 
    Details
    ISSN: 1432-0428
    Keywords: Key words Copper ; interleukin-1β ; islets ; insulin secretion ; glucose metabolism ; nitric oxide.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since copper [Cu(II)] is a necessary cofactor for both intra-mitochondrial enzymes involved in energy production and hydroxyl scavenger enzymes, two hypothesised mechanisms for action of interleukin-Iβ (IL-1β), we studied whether Cu(II) addition could prevent the inhibitory effect of IL-1β on insulin release and glucose oxidation in rat pancreatic islets. Islets were incubated with or without 50 U/ml IL-1β, in the presence or absence of various concentrations of Cu(II)-GHL (Cu(II) complexed with glycyl-l-histidyl-l-lysine, a tripeptide known to enhance copper uptake into cultured cells). CuSO4 (1–1000 ng/ml) was used as a control for Cu(II) effect when present as an inorganic salt. At the end of the incubation period, insulin secretion was evaluated in the presence of either 2.8 mmol/l (basal insulin secretion) or 16.7 mmol/l glucose (glucose-induced release). In control islets basal insulin secretion was 92.0 ± 11.4 pg · islet–1· h–1 (mean ± SEM, n = 7) and glucose-induced release was 2824.0 ± 249.0 pg · islet–1· h–1. In islets pre-exposed to 50 U/ml IL-1β, basal insulin release was not significantly affected but glucose-induced insulin release was greatly reduced (841.2 ± 76.9, n = 7, p 〈 0.005). In islets incubated with IL-1β and Cu-GHL (0.4 μmol/l, maximal effect) basal secretion was 119.0 ± 13.1 pg · islet–1· h–1 and glucose-induced release was 2797.2 ± 242.2, (n = 7, p 〈 0.01 in respect to islets exposed to IL-1β alone). In contrast to data obtained with Cu(II)-GHL, increasing concentrations of CuSO4 (up to 10 μmol/l) did not influence the inhibitory effect of IL-1β on glucose-stimulated insulin release. Glucose oxidation (in the presence of 16.7 mmol/l glucose) was 31.5 ± 2.4 pmol · islet–1· 90min–1 in control islets and 7.0 ± 0.9 (p 〈 0.01) in IL-1β-exposed islets. In islets exposed to IL-1β and Cu-GHL glucose oxidation was similar to control islets (31.9 ± 1.9). In contrast, Cu-GHL did not prevent the IL-1β-induced increase in nitric oxide production. Nitrite levels were 5 ± 1.7, 26 ± 5 and to 29 ± 4 pmol · islet–1· 48 h–1 (mean ± SEM, n = 5) in the culture medium from control, IL-1β and IL-1β + Cu-GHL exposed islets, respectively. These data indicate that the Cu(II) complexed to GHL is able to prevent the inhibitory effects of IL-1β on insulin secretion and glucose oxidation, but not on NO production. The mechanism of action of Cu-GHL is still unclear, but it might restore the activity of the enzymatic systems inhibited by IL-1β. [Diabetologia (1995) 38: 39–45]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050251
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  • 9
    Electronic Resource
    Electronic Resource
    Insulin receptor tyrosine kinase activity is reduced in monocytes from non-obese normoglycaemic insulin-resistant subjects (1993)
    Springer
    Diabetologia 36 (1993), S. 1163-1167 
    Details
    ISSN: 1432-0428
    Keywords: Insulin receptor ; tyrosine kinase ; internalization ; insulin resistance ; human monocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin sensitivity has been quantified by i. v. insulin tolerance test (0.1 U/kg of body weight) in 18 (11 male/7 female) non-obese (body mass index range 19–25 kg/m2) normoglycaemic subjects. We then compared the tyrosine kinase activity and internalization of insulin receptor in monocytes from the six most insulin-sensitive (group 1) and the six most insulin-resistant (group 3) subjects. Tyrosine kinase activity was measured on immunopurified receptors using 32P-ATP and poly-glutamic acid 4: tyrosine 1, sodium salt (poly-glu-tyr 4∶1). Insulin internalization was studied by incubating cells with 1 nmol/l 125I-insulin and measuring total cell-bound and intracellular 125I-insulin by an acid dissociation procedure. Basal (in the absence of insulin) receptor kinase activity was similar in both groups. Maximal (in the presence of 100 nmol/l insulin) kinase activity was 41% lower in group 3 (13.8±3.6 fmoles 32P-ATP incorporated vs 23.3±4.0, p=0.1). Delta increment of receptor kinase activity after insulin stimulation (calculated by subtracting basal from maximal activity) was significantly (p〈0.05) reduced in group 3 (21.3±3.8 vs 11.1±2.1) and significantly (p〈0.05) correlated to the in vivo insulin sensitivity. Both total cell-bound (0.70±0.09 % of total radioactivity added vs 0.83±0.15) and intracellular (0.39±0.05 vs 0.44±0.09) 125I-insulin were similar in the two groups. These data suggest that in non-obese, normoglycaemic subjects a defective insulin receptor tyrosine kinase activity may contribute to the development of insulin resistance. This raises the possibility that the reduced receptor kinase activity observed in Type 2 (non-insulin-dependent) diabetic patients may be independent from the diabetes and may in fact precede the appearance of the disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401061
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  • 10
    Electronic Resource
    Electronic Resource
    Increased adipose tissue PC-1 protein content, but not tumour necrosis factor-a gene expression, is associated with a reduction of both whole body insulin sensitivity and insulin receptor tyrosine-kinase activity (1997)
    Springer
    Diabetologia 40 (1997), S. 282-289 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Adipose tissue ; insulin sensitivity ; insulin tolerance test ; insulin receptor tyrosine-kinase inhibitors ; tumour necrosis factor-α ; PC-1.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the present study we measured PC-1 content, tumour necrosis factor (TNF)-α gene expression, and insulin stimulation of insulin receptor tyrosine-kinase activity in adipose tissue from non-obese, non-diabetic subjects. These parameters were correlated with in vivo insulin action as measured by the intravenous insulin tolerance test (Kitt values). PC-1 content was negatively correlated with Kitt values (r = –0.5, p = 0.04) and positively with plasma insulin levels both fasting (r = 0.58, p = 0.009) and after 120 min during oral glucose tolerance test (OGTT) (r = 0.67, p = 0.002). Moreover, adipose tissue PC-1 content was higher in relatively insulin-resistant subjects (Kitt values lower than 6) than in relatively insulin-sensitive subjects (Kitt values higher than 6) (525 ± 49 ng/mg protein vs 336 ± 45, respectively, p = 0.012). Adipose tissue insulin receptor tyrosine-kinase activity in response to insulin was significantly lower at all insulin concentrations tested (p = 0.017, by two-way analysis of variance test) in insulin-resistant than in insulin-sensitive subjects (Kitt values lower or higher than 6, respectively). In contrast to PC-1, no significant correlation was observed between adipose tissue TNF-α mRNA content and Kitt values, and plasma insulin levels, both fasting and at after 120 min during OGTT. Also, no difference was observed in TNF-α mRNA content between subjects with Kitt values higher or lower than 6. These studies in adipose tissue, together with our previous studies in skeletal muscle raise the possibility that PC-1, by regulating insulin receptor function, may play a role in the degree of insulin sensitivity in non-obese, non-diabetic subjects. [Diabetologia (1997) 40: 282–289]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050675
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