Obesity remains a continuing global health concern and its prevalence has been doubled since 1980 and according to WHO estimates, in 2016, more than 650 million people are obese and 1.9 billion people are overweight [1]. It is associated with increased risk of many chronic diseases including type 2 diabetes (T2D), hypertension, and cardiovascular disease (CVD).
According to WHO, obesity can be defined simply as abnormal or excessive body fat accumulation to such an extent that health may be adversely affected. Body mass index (BMI) is used to classify body fat measurement but without interpretation for the wide difference in the body fat distribution.
Growth hormone and IGF-1 have major role in metabolic regulation, reproduction and aging. It is produced by anterior pituitary gland in response to growth hormone releasing hormone (GHRH) which is released by hypothalamus as normal reflections to multiple features such as hypoglycaemia, low free fatty acid in the blood, high amino acid, good exercise and sleep [2]. All these features are diminished in adult subjects with high BMI [3]. Following an increase in BMI, GH secretion is reduced that will lead to lipid metabolism disturbance, increases body fat, increases T2D and cardiovascular diseases risk.4 Binding of GH to its receptor on the liver, and other organs, stimulates the production of IGF-1 which is secreted and delivered to the target tissues [4]. IGF-1 reflect GH levels and mediates the effects of GH while the metabolic effects of GH are induced directly through its receptor [5]. GH secretion is inhibited by IGF-1 and IGF-1 production is stimulated by GH in a negative feedback mechanism [6]. IGF-1 in the circulation binds to IGF-binding proteins (IGFBPs). These IGFBPs act as transporter proteins, modulate IGF actions and regulate the clearance of IGFs [7]. In obesity, non-esterified fatty acids (NEFA) and insulin will inhibit IGFBP production which increase the free IGF-1 in circulation [8]. Serum IGF-1 are reported to be low in young diabetic subjects [9].
IGFBP-2 is considered to be second most abundant of all and is responsible for several cellular processes like cell proliferation, migration, and adhesion, which play a significant role in the cancer establishment and its succession [10–11]. It is secreted by the differentiation of pre-adipocytes. Plasma IGFBP-2 levels can be used as a biomarker of insulin sensitivity as it helps in glucose metabolism by improving insulin sensitivity [12]. Increased levels of IGFBP2 had strong inverse association with risk of T2DM body mass index [13–14].
Bariatric surgery is an effective treatment for severe obesity that leads to improvement and remission of many obesity-related comorbidities, sustained weight loss over time, improvement in quality of life and prolonged survival [15–16]. Bariatric surgery reduces body weight and improves glycaemic control through reduced nutrient intake and malabsorption. However, there are other mechanisms like changes in the secretion and activity of hormones and neurotransmitters involved in appetite, energy expenditure and glucose metabolism also add to the beneficial effects of bariatric surgery [17–18].
As yet, the underlying mechanisms of how bariatric surgery is influencing the physiological metabolic process pre and post-surgery are not fully understood. Therefore, the aim of this study was to assess the GH/IGF-1 axis and IGFBP-2 levels in obese patients before and after gastric sleeve surgery and correlation with other anthropometric parameters and lipid profile.