Serum RBP4 positively correlates with triglyceride level but not with BMI,fat mass and insulin resistance in healthy obese and non-obese individuals

Abstract

Purpose: Retinol binding protein 4 (RBP4) has recently been identified as an adipokine possibly involved in the development of impaired glucose metabolism. We aimed to test serum RBP4 in healthy non-obese individuals and in patients with well-characterized phenotype: obesity without confounding effects of diabetes, metabolic syndrome or dyslipidaemia. Additionally, we examined whether serum RBP4 is associated with anthropometric parameters, insulin resistance and blood lipid parameters.

Patients and methods: Twenty-eight patients with obesity and no co-morbidities and twenty-five age-matched lean controls were recruited. Anthropometric parameters, body composition, fasting blood lipid profile, RBP4, glucose and insulin were assessed and HOMA-IR was calculated.

Results: Mean concentration of RBP4 did not differ between studied groups (in obese patients was 33.93?±?4.46?µg/ml and 32.53?±?2.53?µg/ml in non-obese controls). RBP4 positively correlated with serum triglycerides in obese and non-obese individuals (r?=?0.74, p?=?0.03 and r?=?0.62, p?=?0.02, respectively) and did not show any significant associations with HOMA-IR, anthropometric and body composition parameters.

Conclusions: Excessive adiposity without co-morbidities is not associated with higher levels of circulating RBP4. Serum RBP4 cannot be considered as a direct predictive marker for impaired glucose metabolism. RBP4 possibly contributes to lipid metabolism.     

Increased circulating IL-8 is associated with reduced IGF-1 and related to poor metabolic control in adolescents with type 1 diabetes mellitus

Background: A dysregulated growth hormone (GH)/insulin-like growth factor 1 (IGF-1) axis is well-recognized in children and adolescents with type 1 diabetes mellitus (T1DM). Decreased IGF-1 levels can also be found in chronic inflammatory diseases, while hyperglycemia promotes inflammatory cytokine production. Therefore, inflammatory cytokines may link poor metabolic control with GH/IGF-1 axis changes. This study examined the relationship between serum inflammatory cytokines and IGF-1 in adolescents (age 13–18) with TIDM in chronic poor (n = 17) or favorable (n = 19) glucose control. Poor control (PC) was defined as 3, consistent HbA1C > 9% during the previous 2 years, while favorable control (FC) was consistent levels of HbA1C < 9%. Results: HbA1C (FC: 7.5 ± 0.6%; PC: 10.5 ± 0.9%, p < 0.001) and interleukin (IL)-8 (FC: 3.7 ± 4.0 pg/ml; PC: 7.4 ± 4.3 pg/ml, p = 0.01) were increased and IGF-1 (FC: 536.5 ± 164.3 ng/ml; PC: 408.9 ± 157.1 ng/ml, p = 0.03) was decreased in patients with poor control compared to patients with favorable control. Moreover, IL-8 was inversely correlated with IGF-1 (r = −0.40, p = 0.03) and positively correlated with HbA1C (r = 0.36, p = 0.03). Conclusions: In adolescents with T1DM and chronic, poor glucose control, increased serum IL-8 is associated with reduced IGF-1 suggesting a pro-inflammatory milieu that may contribute to alterations in the GH/IGF-1 axis.     

Increased body condition score through increased lean muscle,but not fat deposition,is associated with reduced reproductive response to oestrus induction in beef cows

Energy reserve, estimated as body condition score (BCS), is the major determinant of the re-initiation of ovarian activity in postpartum cows. Leptin, IGF-I and insulin are positively related to BCS and are putative mediators between BCS and reproductive function. However, when BCS and body composition dissociates, concentrations of these metabolic hormones are altered. We hypothesized that increasing lean muscle tissue, but not fat tissue, would diminish the reproductive response to oestrus induction treatments. Thirty lactating beef cows with BCS of 3.10±1.21 and 75.94±12 days postpartum were divided in two groups. Control cows (n=15) were supplemented with 10.20 kg of concentrate daily for 60 days. Treated cows (n=15) were supplemented equally, and received a β-adrenergic receptor agonist (β-AA; 0.15 mg/kg BW) to achieve accretion of lean tissue mass and not fat tissue mass. Twelve days after ending concentrate supplementation/β-AA treatment, cows received a progestin implant to induce oestrus. Cows displaying oestrus were inseminated during the following 60 days, and maintained with a fertile bull for a further 21 days. Cows in both groups gained weight during the supplementation period (Daily weight gain: Control=0.75 kg v. β-AA=0.89 kg). Cows treated with β-AA had a larger increase in BCS (i.e. change in BCS: control=1 point (score 4.13) v. β-AA=2 points (score 5.06; P<0.05), as a result of muscle accretion (i.e. change in muscle depth: control 0.21 cm v. β-AA 0.97 cm; P<0.05) but not adipose tissue (i.e. change in back fat depth; control 0.13 cm v. β-AA −0.06 cm; P<0.05). The changes in body composition in β-AA cows were associated with a reduction in serum concentrations of IGF-I (25.4%) and leptin (27.9%), without observed changes in insulin. Ovulation and pregnancy to 1st service (P>0.05) did not differ between groups. However, the number of cows displaying oestrus (control 13/15 v. β-AA 8/15; P<0.05) and the percentage cycling (control 6/8 v. β-AA 3/10; P=0.07) after progestin treatment and the pregnancy percentage at the end of the breeding period (control 13/15 v. β-AA 8/15; P<0.05) were lower in β-AA than control cows. In summary, the increase BCS through muscle tissue accretion, but not through fat tissue accretion, resulted in a lower response to oestrus induction, lower percentage of cycling animals and lower pregnancy percentage after progestin treatment; which was associated with a decrease in serum concentrations of leptin and IGF-I.