| Literature link | GPT Summary | Evidence category | Disease type |
|---|---|---|---|
| 31836012 | This study investigated the role of first-trimester leptin, resistin, and visfatin levels in predicting gestational diabetes mellitus (GDM) among 70 women who developed GDM and 70 controls. Women who later developed GDM exhibited significantly higher levels of leptin, resistin, and visfatin, along with dyslipidemia, compared to those without GDM (p < 0.05). The predictive value of these adipokines was strong, with areas under the ROC curves (AUCs) of 0.812, 0.836, and 0.799 for leptin, resistin, and visfatin, respectively. Increased leptin (OR = 1.166, CI = 1.104–1.233, p < 0.0001), resistin, and visfatin levels were independently associated with GDM. The study concludes that elevated levels of these adipokines in the first trimester may serve as reliable predictive markers for GDM. |
Risk factor |
GDM |
| 14990416 | This study investigated the relationship between maternal plasma leptin concentrations in early pregnancy and the risk of developing gestational diabetes mellitus (GDM). Among 823 women, 5.7% (47) developed GDM. Elevated leptin concentrations at 13 weeks of gestation were significantly associated with an increased risk of GDM (P for trend <.001). After adjusting for maternal pre-pregnancy adiposity and other confounders, women with leptin concentrations ≥31.0 ng/mL had a 4.7-fold increased risk of GDM (95% CI: 1.2–18.0) compared to those with concentrations ≤14.3 ng/mL. A linear trend was observed, with each 10-ng/mL increase in leptin levels corresponding to a 20% increase in GDM risk (RR 1.2, 95% CI: 1.0–1.3). The findings suggest that hyperleptinemia in early pregnancy, independent of maternal adiposity, is predictive of increased GDM risk, warranting further research to confirm its etiological role. |
Risk factor |
GDM |
| 17392604 | Pre-B-cell colony-enhancing factor (PBEF), also known as visfatin, is an adipocytokine found in high levels in visceral fat. It exerts insulin-mimetic effects by binding to and activating the insulin receptor, contributing to metabolic processes. PBEF was initially discovered as a cytokine involved in B-cell differentiation and was later recognized for its role in inhibiting neutrophil apoptosis in sepsis. Although PBEF lacks a signal sequence, it is secreted and involved in regulating inflammatory responses. In addition to its role in inflammation, PBEF/visfatin has been implicated in the pathophysiology of labor, colorectal cancer, and cell cycle regulation. Intracellularly, PBEF/visfatin functions as a cytosolic enzyme crucial for nicotinamide adenine dinucleotide (NAD) synthesis, particularly important for vascular smooth muscle cell maturation. This review summarizes the broad functions and pathophysiological implications of PBEF/visfatin, emphasizing its potential involvement in various diseases and its evolutionary conservation across species. | Mechanism | Insulin resistance |
| 9732873 | Nutritional deprivation suppresses immune function, and the discovery of the obese gene and its protein product, leptin, has provided crucial insights into the hypothalamic regulation of body weight. Leptin, an adipocyte-derived hormone, is directly proportional to fat mass but can decrease rapidly during fasting or increase due to inflammatory mediators. Despite the recognition that impaired T-cell immunity occurs in mice lacking leptin (ob/ob) or its receptor (db/db), the underlying mechanism has not been fully explained. Additionally, reduced leptin levels and impaired cell-mediated immunity are also associated with low body weight in humans, and malnutrition increases susceptibility to infectious diseases. This study reveals that leptin specifically influences T-lymphocyte responses, enhancing naive T-cell proliferation while suppressing memory T-cell activity. Leptin also promotes Th1 cytokine production while inhibiting Th2 cytokines. Administration of leptin to mice counteracted the immunosuppressive effects of acute starvation. These findings propose that leptin plays a vital role in linking nutritional status with cellular immune function, offering a molecular mechanism for the immune dysfunction observed during starvation | Mechanism | Inflammatory |
| 35985429 | This nested case-control study examined the relationship between early pregnancy adiponectin, leptin, and the leptin/adiponectin ratio (LAR) and the risk of gestational diabetes mellitus (GDM) in 332 GDM cases and 664 matched controls from the Tongji-Shuangliu Birth Cohort. Higher adiponectin levels were associated with a reduced GDM risk (OR 0.55 for the highest vs. lowest quartile), while higher leptin levels (OR 1.96) and LAR (OR 2.72) were associated with increased GDM risk (all p-trend < 0.02). Adding adiponectin and leptin to a conventional prediction model slightly improved its predictive ability (C-statistic increased from 0.708 to 0.728) and yielded a net reclassification improvement of 0.292. The study concludes that adiponectin is inversely associated with GDM risk, while leptin and LAR are positively associated, suggesting these biomarkers may enhance early GDM risk prediction in Chinese pregnant women. | Risk factor | GDM |
RF's name
Leptin
RF's type
Adipocyte factor