Circulating obestatin levels and the ghrelin/obestatin ratio in obese women

Abstract

Objective: We measured blood levels of obestatin, total ghrelin, and the ghrelin/obestatin ratio and their relationship with anthropometric and metabolic parameters, adiponectin and insulin resistance, in overweight/obese and normal-weight women. Design: Outpatients Unit of Endocrinology of the S Orsola-Malpighi Hospital of Bologna, Italy. Methods: Fasting obestatin, ghrelin, adiponectin and lipid levels, fasting and glucose-stimulated oral glucose tolerance test insulin, and glucose levels were measured in 20 overweight/obese and 12 controls. The fasting ghrelin/obestatin ratio was calculated; the homeostasis model assessment-IR (HOMA-IR) and insulin sensitivity index (ISI composite ) were calculated as indices of insulin resistance. Results: Obese women had higher obestatin and lower ghrelin blood levels, and a lower ghrelin/obestatin ratio compared with controls. In all subjects, obestatin was significantly and positively correlated with total cholesterol and triglycerides, but not with ghrelin, anthropometric, and metabolic parameters. In the obese women, however, obestatin and ghrelin concentrations were positively correlated. By contrast, the ghrelin/obestatin ratio was significantly and negatively correlated with body mass index, waist, waist-to-hip ratio, fasting insulin, and HOMA-IR, and positively with ISI composite but not with adiponectin. None of these parameters were correlated with the ghrelin/obestatin ratio in the obese. Conclusions: Increased obestatin, decreased ghrelin levels, and a decreased ghrelin/obestatin ratio characterize obesity in women. This supports the hypothesis that the imbalance of ghrelin and obestatin may have a role in the pathophysiology of obesity. On the other hand, some relevant differences between our data on circulating levels of obestatin and the ghrelin/obestatin ratio in obese subjects and those reported in the few studies published so far imply that further research is needed.European Journal of Endocrinology 157 295-301

Ghrelin Gene Products and the Regulation of Food Intake and Gut Motility

“…Therefore, the assumption that systemic total ghrelin levels reflect acyl ghrelin secretion should be made with caution (Gauna et al, 2007). For instance, fasting plasma total ghrelin (Cummings et al, 2002a;English et al, 2002;Rigamonti et al, 2002;Shiiya et al, 2002;Erdmann et al, 2005;Korner et al, 2005Korner et al, , 2006le Roux et al, 2005b;Engström et al, 2007;Guo et al, 2007;Vicennati et al, 2007;Huda et al, 2009;), des-acyl ghrelin (Rodríguez et al, 2009), and obestatin (Guo et al, 2007;Nakahara et al, 2008) concentration were lower in obese than lean subjects, whereas acyl ghrelin concentration was higher in obese persons (Rodríguez et al, 2009). In addition, obese persons showed lower expression of GHS-R in omental adipose tissue (Rodríguez et al, 2009).…”

Ghrelin Gene Products in Acute and Chronic Inflammation

“…Circulating obestatin concentrations have been reported to be either reduced (Anderwald-Stadler et al 2007;Nakahara et al 2008) or, more frequently, increased (Guo et al 2007;Prodam et al 2011;Reinehr et al 2008;Vicennati et al 2007) in obesity. Based on available data, it is difficult to explain these contrasting findings that seem to depend mainly on sample size, age, and ethnicities.…”

Ghrelin and obestatin levels in hypertensive obese patients

“…6,7 Changes in the concentrations of these hormones, and in the ghrelin/obestatin ratio, may be risk factors for obesity and hypertension. 8 Ghrelin is a peptide hormone secreted primarily from the stomach and duodenum; it is a stimulant of appetite and increases adiposity in rodents. 9 However, many studies have shown that obesity is associated with a decrease in circulating ghrelin.…”

“…15,16 In addition, obestatin has been shown to be positively correlated with ghrelin. 8 This suggests that levels of both obestatin and ghrelin may be altered in obesity and insulin resistance. Obestatin has been reported to decrease vascular cell adhesion molecule-1 expression in endothelial cells when stimulated with tumour necrosis factor-a, and to increase oxidized low-density lipoprotein binding to macrophages.…”