Insulin sensitivity and insulin secretion at birth in intrauterine growth retarded infants

Setia, Sajita; Sridhar, Magadi Gopalakrishna; Bhat, Vishnu; Chaturvedula, Lata; Vinayagamoorti, R.; John, Mathew

doi:10.1080/00313020600696256

Cited by 58 publications

(58 citation statements)

References 14 publications

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“…On the other hand, high cortisol values have been related to insulin resistance early in life [4], suggesting a low prevalence of insulin resistance in the neonatal population tested. The neonatal glucose levels we found concur with those of other studies [29] and were similar in males and females, although those of female neonates tended to be slightly higher (p>0.1) in all quartiles.…”

Section: Discussionsupporting

confidence: 94%

“…To date, few studies determining HOMA or QUICKI have been published [29], and none of these have used HOMA-S on neonates. Moreover, normal ranges have not yet been established for HOMA in term-neonates, for the relationships between cortisol, insulin-like growth factor-1 (IGF-1), growth hormone (GH), glucose and insulin and for the HOMA and QUICKI indexes at birth.…”

Section: Introductionmentioning

confidence: 99%

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Insulin resistance markers in term, normoweight neonates. The Mérida cohort

Gesteiro¹,

Bastida

Sánchez‐Muniz

2008

Eur J Pediatr

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Several endocrine regulators are implicated in the development of metabolic syndrome. The aim of our study was to assess normal ranges for glucose, growth hormone (GH), insulin-like growth factor-1 (IGF-1), cortisol, insulin and the yet-to-be-published quantitative insulin sensitivity check index (QUICKI) for newborns and a number of homeostatic model assessment (HOMA)-related equations that have been proposed as indicators of insulin sensitivity (HOMA-S) and insulin resistance (HOMA-R). The study included 115 (54 males, 61 females) singleton, normoweight, Spanish Caucasian neonates delivered without foetal distress from mothers of the Mérida (Spain) Birth Cohort who tested negative in the O'Sullivan screen. Neonatal normal values given as the mean (95% confidence interval) were: glucose, 75.3 mg/dL (68.29-82.29); cortisol, 7.4 microg/dL (6.85-7.97); GH, 16.7 ng/mL (14.87-18.60); insulin, 5.5 microUI/mL (4.12-6.88), IGF-155.2 ng/mL (50.82-59.53); QUICKI, 0.45 (0.43-0.48); HOMA-R, 1.36 (0.84-1.88); HOMA-S, 4.07 (2.66-5.49), the glucose/insulin ratio, 33.6 (24.58-42.67); the insulin/cortisol ratio, 0.8 (0.61-1.05). Hormone ranges (except for cortisol, whose values were lower) were equivalent to those of other studies. Cortisolaemia values cannot be associated with the type of delivery, as only three births (2.6%) were by caesarean section, while 20 (17.4%) were instrumental deliveries. Neonates from the lowest quartile of the insulin/cortisol ratio presented higher (p < 0.001) HOMA-S and QUICKI and lower (p < 0.01) HOMA-R values. The results of our study indicate normal ranges for insulin resistance and sensitivity at birth. The insulin/cortisol ratio at birth appears to be a good early indicator of insulin resistance.

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Insulin resistance markers in term, normoweight neonates. The Mérida cohort

Gesteiro¹,

Bastida

Sánchez‐Muniz

2008

Eur J Pediatr

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“…In contrast, small size at birth predicts glucose intolerance or diabetes and impaired insulin sensitivity consistently in epidemiological studies of men and women over 40 yr old (20). Together with observations in human IUGR infants and 2-yr-old children (16,35) and in offspring of protein-deprived pregnant rats (27), these results in a range of species suggest that restricted fetal growth is followed initially by improved insulin sensitivity, which switches to insulin resistance with aging. Furthermore, the timing of this switch appears to differ between sexes, occurring by young adulthood in men and later in women.…”

Section: Discussionmentioning

confidence: 52%

Sex-specific effects of placental restriction on components of the metabolic syndrome in young adult sheep

Owens¹,

Thavaneswaran²,

Blasio³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…Similarly, fasting glucose and insulin levels were assessed at baseline and at 12 weeks followup. The insulin indices: leptin/adiponectin ratio (LAR), 11 homeostasis model assessment of insulin resistance (HOMA- 13 for insulin sensitivity were calculated at baseline and at 12 weeks after treatment. For controls, anthropometric measurements were done and single blood sample was collected at time of recruitment for assay of the above-mentioned routine biochemical parameters, adipokine levels and insulin indices.…”

Section: Workupmentioning

confidence: 99%