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1 or using C-peptide level as an indication of hyperinsulinaemia.
2 gressive worsening of hyperphagia-associated hyperinsulinaemia.
3 develop severe hyperandrogenism secondary to hyperinsulinaemia.
4 rgic suppression of fetal glucose-stimulated hyperinsulinaemia.
5 ta-cell proliferation and mass, resulting in hyperinsulinaemia.
6 e opposite of the known short-term effect of hyperinsulinaemia.
7  G4A-/- mice develop glucose intolerance and hyperinsulinaemia.
8 inaemic and male Mc3r(-/-) mice develop mild hyperinsulinaemia.
9 se hyperglycaemia, hypertriglyceridaemia and hyperinsulinaemia.
10 lower colorectal cancer risk than those with hyperinsulinaemia.
11 d is a consequence of hyperphagia-associated hyperinsulinaemia.
12 de, instead of tertiles, as the cut-point of hyperinsulinaemia, a similar pattern of associations was
13 type 2 diabetes, conditions characterised by hyperinsulinaemia and insulin resistance.
14  profound effects, giving rise to congenital hyperinsulinaemia and neonatal diabetes respectively.
15 responses essential to maintain energy flux (hyperinsulinaemia and the suppression of GH release) ove
16 riable coexistence of obesity, dyslipidemia, hyperinsulinaemia, and hypertension.
17 rexpression in the presence of physiological hyperinsulinaemia; and (3) largely unaffected by GLUT4 o
18 t unrestrained de-novo lipogenesis driven by hyperinsulinaemia appears to play an important role.
19            Chronic anovulation, obesity, and hyperinsulinaemia are all associated with PCOS as well a
20 we aimed to examine the potential effects of hyperinsulinaemia associated with high-fat diet (HFD) fe
21 amines and suppression of glucose-stimulated hyperinsulinaemia, but other factors reduce plasma insul
22 hese hormones led to reduced somatic growth, hyperinsulinaemia, glucose intolerance, hyperphagia and
23 ze subtypes categorised by the prevalence of hyperinsulinaemia have been defined, and metabolically h
24 ealthy overweight/obese individuals (without hyperinsulinaemia) have been suggested to be at lower ri
25 or the positive relationship between chronic hyperinsulinaemia, hepatic VLDL-triacylglycerol secretio
26 y a severe resistance to insulin, leading to hyperinsulinaemia, hyperglycaemia and enlarged fatty liv
27 iciency in adipose tissue and liver produces hyperinsulinaemia, impaired glucose tolerance and resist
28  more important barrier during physiological hyperinsulinaemia in all muscles.
29                                      Chronic hyperinsulinaemia in insulin-resistant syndromes results
30  of this switch for the relationship between hyperinsulinaemia, increased hepatic very-low-density li
31             Women with anovulatory PCOS have hyperinsulinaemia, insulin resistance, and dyslipidaemia
32 ith adverse outcomes in prostate cancer, and hyperinsulinaemia is a candidate mediator, but prospecti
33 nt may be more important in conditions where hyperinsulinaemia is secondary to insulin resistance.
34                                      Because hyperinsulinaemia itself is an independent risk factor f
35 uscle wasting, myotonia, cardiac arrhythmia, hyperinsulinaemia, mental retardation and ocular catarac
36              This is driven by the action of hyperinsulinaemia on the liver, mediated by PI3 kinase,
37                              We propose that hyperinsulinaemia promotes growth while suppressing the
38  prevent increased adiposity, but attenuated hyperinsulinaemia, recovered GH release, and normalized
39 dy size phenotypes were defined according to hyperinsulinaemia status using serum concentrations of C
40 f insulin synthesis and secretion leading to hyperinsulinaemia-the hallmark of this disease.

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