Faculty of Medicine, Department of General Surgery, Gazi University, Besevler, Ankara, Turkey.
Mustafa Kemal Mah. 2137. Sok. 8/14, 06520, Cankaya, Ankara, Turkey.
Adv Exp Med Biol. 2024;1460:1-25. doi: 10.1007/978-3-031-63657-8_1.
Increase in the prevalence of obesity has become a major worldwide health problem in adults as well as among children and adolescents. In the last four decades, studies have revealed that the significant increase in the prevalence of obesity has become a pandemic. Obesity is the result of complex interactions between biological, genetic, environmental, and behavioral factors. Indeed, almost all of the children suffering from obesity in early childhood face with being overweight or obese in adolescence. Different phenotypes have different risk factors in the clinical evaluation of obesity. Individuals suffering from metabolically unhealthy obesity (MUO) are at an excess risk of developing cardiovascular diseases (CVDs), several cancer types, and metabolic syndrome (MetS), whereas the metabolically healthy obesity (MHO) phenotype has a high risk of all-cause mortality and cardiometabolic events but not MetS. While most obese individuals have the MUO phenotype, the frequency of the MHO phenotype is at most 10-20%. Over time, approximately three-quarters of obese individuals transform from MHO to MUO. Total adiposity and truncal subcutaneous fat accumulation during adolescence are positively and independently associated with atherosclerosis in adulthood. Obesity, in general, causes a large reduction in life expectancy. However, the mortality rate of morbid obesity is greater among younger than older adults. Insulin resistance (IR) develops with the central accumulation of body fat. MHO patients are insulin-sensitive like healthy normal-weight individuals and have lower visceral fat content and cardiovascular consequences than do the majority of MUO patients. MetS includes clustering of abdominal obesity, dyslipidemia, hyperglycemia, and hypertension. The average incidence of MetS is 3%, with a 1.5-fold increase in the risk of death from all causes in these patients. If lifestyle modifications, dietary habits, and pharmacotherapy do not provide any benefit, then bariatric surgery is recommended to reduce weight and improve comorbid diseases. However, obesity treatment should be continuous in obese patients by monitoring the accompanying diseases and their consequences. In addition to sodium-glucose co-transporter-2 (SGLT2) inhibitors, the long-acting glucagon-like peptide-1 (GLP-1) receptor agonist reduces the mean body weight. However, caloric restriction provides more favorable improvement in body composition than does treatment with the GLP-1 receptor (GLP1R) agonist alone. Combination therapy with orlistat and phentermine are the US Food and Drug Administration (FDA)-approved anti-obesity drugs. Recombinant leptin and synthetic melanocortin-4-receptor agonists are used in rarely occurring, monogenic obesity, which is due to loss of function in the leptin-melanocortin pathway.
肥胖症的患病率在成年人、儿童和青少年中都呈上升趋势，已成为全球主要的健康问题。在过去的四十年中，研究表明肥胖症的显著增加已成为一种全球性的流行疾病。肥胖是生物、遗传、环境和行为因素之间复杂相互作用的结果。事实上，几乎所有在儿童早期肥胖的儿童在青春期都面临超重或肥胖的问题。不同的表型在肥胖的临床评估中有不同的危险因素。患有代谢不健康型肥胖症（MUO）的个体患心血管疾病（CVD）、多种癌症类型和代谢综合征（MetS）的风险过高，而代谢健康型肥胖症（MHO）的表型患全因死亡率和心血管代谢事件的风险较高，但没有 MetS。虽然大多数肥胖者表现为 MUO 表型，但 MHO 表型的频率最多为 10-20%。随着时间的推移，大约四分之三的肥胖者从 MHO 转变为 MUO。青春期总脂肪量和躯干皮下脂肪堆积与成年期动脉粥样硬化呈正相关且独立相关。肥胖总体上会导致预期寿命大幅缩短。然而，与老年人相比，年轻的病态肥胖者死亡率更高。胰岛素抵抗（IR）随着身体脂肪的中心堆积而发展。MHO 患者与健康的正常体重个体一样对胰岛素敏感，并且内脏脂肪含量和心血管后果低于大多数 MUO 患者。代谢综合征包括腹部肥胖、血脂异常、高血糖和高血压的聚集。代谢综合征的平均发病率为 3%，这些患者的全因死亡风险增加 1.5 倍。如果生活方式改变、饮食习惯和药物治疗没有带来任何益处，那么建议进行减重手术以减轻体重并改善合并症。然而，肥胖患者应通过监测伴随疾病及其后果，持续进行肥胖治疗。除了钠-葡萄糖协同转运蛋白-2（SGLT2）抑制剂外，长效胰高血糖素样肽-1（GLP-1）受体激动剂还可减轻体重。然而，与单独使用 GLP-1 受体（GLP1R）激动剂相比，热量限制可更有利地改善身体成分。奥利司他和苯丁胺的联合治疗是美国食品和药物管理局（FDA）批准的抗肥胖药物。重组瘦素和合成黑皮质素-4 受体激动剂用于罕见的单基因肥胖症，这是由于瘦素-黑皮质素途径功能丧失所致。
