<p><i>Helicobacter</i> <i>pylori</i> (<i>H. pylori</i>) infection is a recognized risk factor for gastric cancer (GC), which is the leading cause of cancer-related deaths worldwide. As a Class I carcinogen, <i>H. pylori</i> plays a central role in the occurrence and development of GC. Recent studies have highlighted the critical role of metabolic reprogramming inthe&#xa0;gastric cancer, and <i>H. pylori</i> infection has been shown to significantly alter metabolic pathways in gastric cancer. This review explores the mechanisms by which <i>H. pylori</i> infection drives metabolic changes in GC, particularly in glycolysis, lipid metabolism, and amino acid metabolism. By altering these metabolisms, <i>H. pylori</i> enhances the survival, proliferation, and metastasis of tumor cells, and also promotes immune evasion. Therefore, understanding the ways in which <i>H. pylori</i>-induced metabolic reprogramming of GC cells is essential for identifying new therapeutic targets. By summarizing the latest research progress of these metabolic pathways, new strategies and directions can be provided for gastric cancer treatment.</p> Graphical abstract <p></p> <p><i>H. pylori</i> regulates glycolysis, amino acid, and lipid metabolism to facilitate the occurrence and development of gastric cancer.</p>