Diabetes mellitus comprises a group of metabolic abnormalities due to insulin deficiency and/or resistance. Obesity contributes to diabetes, with a strong causal relationship existing between diabetes and insulin resistance, especially in patients with Diabetes mellitus II. Adipocytes emerge as key constituents of adipose tissue physiology. In their pre-mature form to mature state transformation, adipocytes fully exemplify one of the key adipogenic actions of insulin. Poised to a) gain insight into adipogenesis leading to antidiabetic factors, and b) investigate adipogenesis through careful examination of insulin contributions to interwoven mechanistic pathways, a systematic comparative study was launched involving well-defined metal-citrates (zinc and vanadium), the chemical reactivity of which was in line with their chemistry under physiological conditions. Selection of the specific compounds was based on their common aqueous coordination chemistry involving the physiological chelator citric acid. Cellular maturation of pre-adipocytes to their mature form was pursued in the presence-absence of insulin and employment of closely linked genetic targets, key to adipocyte maturation (Peroxisome proliferator-activated receptor gamma (PPAR-γ), Glucose transporter 1,3,4 (GLUT 1,3,4), Adiponectin (ADIPOQ), Glucokinase (GCK), and Insulin receptor (INS-R)). The results show a) distinct adipogenic biological profiles for the metalloforms involved in a dose-, time- and nature-dependent manner, and b) metal ion-specific adipogenic response-signals at the same or higher level than insulin toward all selected targets. Collectively, the foundations have been established for future exploitation of the distinct metal-specific adipogenic factors contributing to the functional maturation of adipose tissue and their use toward hyperglycemic control in Diabetes mellitus.

糖尿病包括由于胰岛素缺乏和/或抗性而引起的一组代谢异常。肥胖会导致糖尿病，在糖尿病和胰岛素抵抗之间存在很强的因果关系，尤其是在患有II型糖尿病的患者中。脂肪细胞是脂肪组织生理学的关键组成部分。脂肪细胞以其过早的形式向成熟的状态转化，充分体现了胰岛素的关键成脂作用之一。准备好：a）深入了解导致糖尿病因素的脂肪形成，b）通过仔细检查胰岛素对交织机制途径的贡献来研究脂肪形成，开展了系统的比较研究，涉及明确的金属柠檬酸盐（锌和钒），其化学反应性与其在生理条件下的化学反应相符。具体化合物的选择基于其常见的涉及生理螯合剂柠檬酸的水配位化学。在不存在胰岛素和使用紧密联系的遗传靶标（脂肪酶增殖物激活受体γ（PPAR-γ），葡萄糖转运蛋白1,3， 4（GLUT 1,3,4），脂联素（ADIPOQ），葡糖激酶（GCK）和胰岛素受体（INS-R））。结果显示：a）以剂量，时间和自然依赖性方式参与的金属型的独特的成脂生物学特征，以及b）对所有选定靶标的金属离子特异性成脂反应信号的水平与胰岛素相同或更高。