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1 und it developed obesity, hyperglycaemia and hyperinsulinaemia.
2 d is a consequence of hyperphagia-associated hyperinsulinaemia.
3 or using C-peptide level as an indication of hyperinsulinaemia.
4 gressive worsening of hyperphagia-associated hyperinsulinaemia.
5 develop severe hyperandrogenism secondary to hyperinsulinaemia.
6 rgic suppression of fetal glucose-stimulated hyperinsulinaemia.
7 ta-cell proliferation and mass, resulting in hyperinsulinaemia.
8 e opposite of the known short-term effect of hyperinsulinaemia.
9  G4A-/- mice develop glucose intolerance and hyperinsulinaemia.
10 inaemic and male Mc3r(-/-) mice develop mild hyperinsulinaemia.
11 se hyperglycaemia, hypertriglyceridaemia and hyperinsulinaemia.
12 out impacting systemic insulin resistance or hyperinsulinaemia.
13 lower colorectal cancer risk than those with hyperinsulinaemia.
14 de, instead of tertiles, as the cut-point of hyperinsulinaemia, a similar pattern of associations was
15 s, marked by systemic insulin resistance and hyperinsulinaemia, along with characteristics of metabol
16 f adipokines and pro-inflammatory cytokines, hyperinsulinaemia and insulin resistance, which exert di
17 type 2 diabetes, conditions characterised by hyperinsulinaemia and insulin resistance.
18                                  We focus on hyperinsulinaemia and its consequences: acutely impaired
19  profound effects, giving rise to congenital hyperinsulinaemia and neonatal diabetes respectively.
20 responses essential to maintain energy flux (hyperinsulinaemia and the suppression of GH release) ove
21 th no change to systemic insulin resistance, hyperinsulinaemia, and elevated triglycerides.
22 riable coexistence of obesity, dyslipidemia, hyperinsulinaemia, and hypertension.
23 rexpression in the presence of physiological hyperinsulinaemia; and (3) largely unaffected by GLUT4 o
24 t unrestrained de-novo lipogenesis driven by hyperinsulinaemia appears to play an important role.
25            Chronic anovulation, obesity, and hyperinsulinaemia are all associated with PCOS as well a
26 we aimed to examine the potential effects of hyperinsulinaemia associated with high-fat diet (HFD) fe
27          Additionally, Cort treatment led to hyperinsulinaemia, but compared to controls, Cort-treate
28 amines and suppression of glucose-stimulated hyperinsulinaemia, but other factors reduce plasma insul
29                                        Fetal hyperinsulinaemia can affect the development of multiple
30 hese hormones led to reduced somatic growth, hyperinsulinaemia, glucose intolerance, hyperphagia and
31 ze subtypes categorised by the prevalence of hyperinsulinaemia have been defined, and metabolically h
32 ealthy overweight/obese individuals (without hyperinsulinaemia) have been suggested to be at lower ri
33 or the positive relationship between chronic hyperinsulinaemia, hepatic VLDL-triacylglycerol secretio
34 y a severe resistance to insulin, leading to hyperinsulinaemia, hyperglycaemia and enlarged fatty liv
35  metabolic abnormalities, including obesity, hyperinsulinaemia, hyperglycaemia and hyperlipidaemia.
36 iciency in adipose tissue and liver produces hyperinsulinaemia, impaired glucose tolerance and resist
37  more important barrier during physiological hyperinsulinaemia in all muscles.
38                                      Chronic hyperinsulinaemia in insulin-resistant syndromes results
39  of this switch for the relationship between hyperinsulinaemia, increased hepatic very-low-density li
40             Women with anovulatory PCOS have hyperinsulinaemia, insulin resistance, and dyslipidaemia
41 ith adverse outcomes in prostate cancer, and hyperinsulinaemia is a candidate mediator, but prospecti
42 nt may be more important in conditions where hyperinsulinaemia is secondary to insulin resistance.
43                                      Because hyperinsulinaemia itself is an independent risk factor f
44 diabetes worldwide, and the realization that hyperinsulinaemia may contribute to therapeutic failures
45 uscle wasting, myotonia, cardiac arrhythmia, hyperinsulinaemia, mental retardation and ocular catarac
46 t we find a strong inverse genetic effect of hyperinsulinaemia on glycine.
47              This is driven by the action of hyperinsulinaemia on the liver, mediated by PI3 kinase,
48                              We propose that hyperinsulinaemia promotes growth while suppressing the
49  prevent increased adiposity, but attenuated hyperinsulinaemia, recovered GH release, and normalized
50 dy size phenotypes were defined according to hyperinsulinaemia status using serum concentrations of C
51 order associated with insulin resistance and hyperinsulinaemia that is insufficient to maintain norma
52 f insulin synthesis and secretion leading to hyperinsulinaemia-the hallmark of this disease.