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Growth hormone (GH) secretion by the pituitary is regulated by stimulatory and inhibitory pathways such as growth hormone releasing hormone (GHRH) and somatostatin, respectively, being also modulated by different neurotransmitters acting at the hypothalamic/pituitary level. The pineal gland hormone melatonin regulates GH secretion in many mammals, including humans, although its role in modulating GH secretion has been debated. We describe the case of a young woman chronically taking melatonin for sleep disturbances, referring to her general practitioner for flushing that appeared just after starting melatonin intake. Laboratory findings showed elevated plasma levels of GH and insulin-like growth factor-1 (IGF-1). She did not show clinical features resembling acromegaly. The evaluation of pituitary and pituitary end organ hormones showed normal plasma levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), estradiol, free thyroid hormones, cortisol, and prolactin. Urinary 5-hydroxyindoleacetic acid levels were normal. One month after melatonin withdrawal, her plasma levels of GH, together with IGF-1, completely normalized. An oral glucose suppression test showed a normal response of GH secretion, further excluding an autonomous secretion. Physicians should be aware of the possible interference of melatonin on GH secretion to prevent misleading diagnosis of autonomous secretion thus avoiding valueless and costly clinical investigations., (© The Author(s) 2025. Published by Oxford University Press on behalf of the Endocrine Society.)

Extracellular ATP exerts important functions as an extracellular signaling molecule via the activation of specific P2 purinergic receptors (P2X and P2Y). We investigated the expression of the different P2 receptors and their possible functional activation in human adipocytes in primary culture. We performed molecular expression analysis of the P2 receptors in human mature adipocytes; examined their functional activation by different nucleotides evaluating [Ca 2+ ] i modifications and IL-6 secretion, and determined the ability of adipocytes to release ATP in the extracellular medium. Human adipocytes express different P2X and P2Y receptors. Extracellular ATP elicited a rise in [Ca 2+ ] i via the activation of P2X and P2Y receptor subtypes. Human adipocytes spontaneously released ATP in the extracellular medium and secreted IL-6 both at rest and after stimulation with ATP. This stimulatory effect of ATP on IL-6 secretion was inhibited by pre-incubation with apyrase, an ATP metabolizing enzyme. These results demonstrate that human adipocytes express different P2X and P2Y receptors that are functionally activated by extracellular nucleotides. Furthermore, human adipocytes spontaneously release ATP, which can act in an autocrine/paracrine fashion on adipocytes, possibly participating in the regulation of inflammatory cytokine release. Thus, P2 purinergic receptors could be a potential therapeutic target to contrast the inflammatory and metabolic complications characterizing obesity.

Fewer studies compared the improvement of plasma lipid levels after different types of surgery, in particular compared to one-anastomosis gastric bypass (OAGB). The aim of our study was to investigate how laparoscopic sleeve gastrectomy (LSG) and OAGB impact on weight loss and lipid profile 18 months after surgery, in patients with severe obesity. Forty-six patients treated with OAGB were matched to eighty-eight patients submitted to LSG. Weight loss after OAGB (33.2%) was more evident than after LSG (29.6%) ( p = 0.024). The difference in the prevalence of dyslipidemia showed a statistically significant reduction only after OAGB (61% versus 22%, p < 0.001). After adjustment for delta body mass index (BMI), age and sex, we demonstrated a statistically significant decrease of the differences between the changes before and after (delta Δ) the two surgery procedures: Δ total cholesterol values ( p < 0.001), Δ low density lipoprotein-cholesterol values ( p < 0.001) and Δ triglycerides values ( p = 0.007). Patients with severe obesity undergoing to OAGB presented a better improvement of lipid plasma values than LSG patients. The reduction of lipid plasma levels was independent of the significant decrease of BMI after surgery, of age and of sex.

A definitive relationship between adiposity and MP production is yet to be demonstrated. The aim of our study was to prospectively evaluate the levels of microparticles (MP) in a group of 20 III degree obese patients before and after weight loss. Plasma levels of annexin V-MP, endothelial-derived MP, platelet-derived MP (CD61+ and P-Selectin+), leukocyte-derived MP, tissue factor-bearing (TF+) and CD36+MP were prospectively measured in 20 patients with III degree obesity (BMI ≥ 40 kg/m(2)) before (T0) and 3 (T3) and 12 (T12) months after sleeve gastrectomy (SLG). Obese patients had lost 18 % of their body weight at T3 and 41 % at T12. We find that considering all MP, except for endothelial-derived MP, which had significantly decreased at T3, all MP subtypes had significantly decreased at T12. At T12, subjects showed a higher median level of all types of MP, except endothelial-derived MP, compared to T3, but without a statistically significant difference. The percentages of reduction of all the MP were significantly correlated with the percentage of reduction of BMI. The reductions of leukocyte-derived, TF+ and CD36+MP were significantly correlated with the reduction of leptin. Moreover, the reductions of leukocyte-derived and CD36+MP were significantly correlated with hs-CRP decrease. The decrease of BMI post-SLG in morbid obesity was matched with a decrease of circulating MP of endothelial, platelet, leukocyte origin, TF+ and CD36+. A trend of slight increase in all MP subtypes, except endothelial-derived, was detected 12 months after gastrectomy, indicating a possible underlying slow low-grade inflammatory/hypercoagulability state from adipose tissue before the potential overt weight gain.

Introduction: Obesity has been associated with hypercoagulability and to increased risk of both arterial and venous thromboembolic events. Many different and complex changes in plasma coagulation factors have been described in patients with obesity. The aim of this case-control study is to evaluate hypercoagulability in a group of overweight and obese subjects by whole blood rotation thromboelastometry (ROTEM®) and impedance aggregometry (Multiplate®)., Methods: ROTEM® and Multiplate® analyses were performed in 80 subjects with a BMI ≥ 25 Kg/m(2), of whom 20 overweight [BMI = 25-29.9 Kg/m(2)], 20 with I degree obesity [BMI = 30-34.9 Kg/m(2)], 20 with II degree obesity [BMI = 35-39.9 Kg/m(2)] and 20 with III degree [BMI > 40 Kg/m(2)] and compared with 80 age and gender-matched normal weight healthy individuals., Results: Thromboelastometry. In INTEM and EXTEM tests MCF and AUC were significantly increased in III degree obese compared with controls. MCF in FIBTEM was significantly higher in I, II and III degree obesity than controls (p = 0.027, 0.002 and < 0.001, respectively). Impedance aggregometry. A significant difference in platelet aggregation was found between III degree obese subjects and healthy controls in each of the tests considered. A significant correlation between FIBTEM-MCF and aggregometry parameters with BMI, waist circumference, leptin levels and high sensitive-C reactive proteins was also found., Conclusions: A relationship between hypercoagulability detected by whole blood thromboelastometry and aggregometry and increased fat mass is shown. Hypercoagulability also correlated with inflammatory markers. Point-of-care tests can be used to assess the degree of hypercoagulability and hyperaggregability in obese patients. Wider studies are needed to confirm our observations., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

The role of circulating microparticles (MP) of different origin and tissue factor (TF)-bearing in overweight and obese patients with and without metabolic syndrome is still a matter of debate. In a case-control study, the presence of hypercoagulability was evaluated in overweight and obese patients by measuring MP, thrombin generation (TG) and FVIIa-AT complexes. Twenty overweight patients (body mass index [BMI] range 25-29.9 kg/m²), 20 with I degree (30-34.9 kg/m²), 20 with II degree (35-39.9 kg/m²) and 20 with III degree obesity (≥ 40 kg/m²) were enrolled and compared to 40 age and gender-matched normal weight individuals. A significant increase in median levels of all MP subtypes was observed in the three degrees of obese patients compared to controls. Overweight patients had higher levels of annexin V-MP (AMP), endothelial-derived, leukocyte-derived and TF-bearing MP than controls. Obese patients had a significantly shorter median lag time (p< 0.05), higher median peak thrombin (p< 0.01) and increased median endogenous thrombin potential [ETP] (p< 0.001) compared to controls. Overweight subjects had significantly increased ETP compared to controls (p< 0.05). Both AMP levels and ETP were found to positively correlate with BMI, waist circumference, and inflammatory parameters. No significant increase in FVIIa-AT complex was seen in cases compared to controls. We conclude that obesity is associated with overproduction of procoagulant MP and increase TG. Interestingly, hypercoagulability is found in overweight patients free of metabolic syndrome and increases with the severity of obesity. Assessment of MP and TG may be helpful in the early characterisation of the prothrombotic state in obese patients.