glucose and lipid metabolism

Overview

Glucose and lipid metabolism refers to the interconnected biochemical processes that regulate the uptake, storage, utilization, and breakdown of carbohydrates and lipids. These pathways are central to energy homeostasis in nearly all tissues, with tight coordination between insulin signaling, fatty acid synthesis and oxidation, glycolysis, gluconeogenesis, and lipoprotein handling. Because glucose and lipid metabolism are coupled at multiple regulatory nodes, disturbances in one arm often affect the other, contributing to metabolic syndrome, obesity, type 2 diabetes, cardiovascular disease, fatty liver disease, and cancer-associated metabolic reprogramming.

In biomedical research, glucose and lipid metabolism is frequently studied as a disease-modifying process rather than as a single pathway. Recent work has linked dysregulated lipid metabolism to tumor aggressiveness, chemoresistance, ferroptosis, and differentiation state in cancers such as breast cancer, glioma, hepatocellular carcinoma, neurofibroma, and other solid tumors. At the same time, altered glucose metabolism has been investigated in inflammatory disease and type 2 diabetes, including studies involving PPARγ-mediated glucose metabolism, obesity-related metabolic disorders, and anesthetic effects in diabetic settings. These findings underscore the role of glucose and lipid metabolism as a shared mechanistic axis connecting metabolic, inflammatory, and malignant phenotypes.

Focus of Latest Publications

Recent publications have examined glucose and lipid metabolism as a dynamic biological process linked to disease progression, immune regulation, and therapeutic response across several contexts. In prostate cancer, multi-omics integration with single-cell RNA sequencing, spatial transcriptomics, and machine learning was used to map lipid metabolic reprogramming and identify prognostic hub genes. This work showed marked heterogeneity in lipid metabolic activity across tumor cell populations, with epithelial and endothelial clusters showing the highest scores, and highlighted central regulators of fatty acid and cholesterol metabolism, including HMGCR, MVK, STARD3, FADS1, and APOE. Spatial analyses further indicated region-specific enrichment of fatty acid biosynthesis and β-oxidation pathways, supporting the view that lipid metabolism reprogramming contributes to prostate cancer progression and therapeutic resistance.

Other studies focused on lipid metabolism as a marker of tumor aggressiveness and membrane remodeling. In glioma, transcriptomic data from The Cancer Genome Atlas were integrated with experimental lipidomic data from glioblastoma cell lines to assess 743 lipid-related genes, identify 29 prognosis-associated genes, and build a risk signature. The study linked higher aggressiveness to altered membrane composition, including increased phospholipids and reduced cholesterol and fatty acid unsaturation, and also implicated sphingolipid signaling, with SMPD1 and SPHK1 emerging as key factors. In HBV-induced macrophages, multi-omics and functional analyses revealed broad lipid metabolic reprogramming alongside acetylation changes, including reduced phosphatidylcholines, phosphatidylinositols, and oxidized lipids, with increased specific sphingolipids and triacylglycerols, suggesting that altered lipid handling contributes to an immunosuppressive macrophage phenotype.

Glucose metabolism was directly investigated in immune and inflammatory disease. Using a few-shot learning and transfer learning screening strategy, one study identified lutein as a selective immunomodulatory candidate that activates PPARγ, suppresses glucose uptake and glycolysis, and inhibits Th1 differentiation in ulcerative colitis models. This work connected glucose metabolism to T cell function and showed that metabolic suppression could alleviate colitis-associated tissue damage. In parallel, a multi-omics study of the diabetic human heart aimed to define the molecular landscape of diabetic cardiomyopathy and reported coupled dysregulation in lipid metabolism, mitophagy, and extracellular matrix remodeling, underscoring the broader metabolic disturbances associated with type 2 diabetes.

Across these studies, glucose and lipid metabolism were repeatedly analyzed using computational tools, multi-omics profiling, transcriptomics, lipidomics, and machine learning approaches to uncover disease-associated metabolic signatures. The findings consistently point to metabolic reprogramming as a central feature of cancer, chronic infection, and inflammatory disease, with potential utility for prognosis, biomarker development, and therapeutic targeting.

Key Publications

NEWJun Machine Learning-Based single-cell characterization of lipid metabolic reprogramming in prostate cancer. (Computers in biology and medicine, 2026, PMID 42361409): "...to characterize lipid metabolism-related gene expression in prostate cancer."
May Multi-omics profiling of the diabetic human heart reveals coupled dysregulation in lipid metabolism, mitophagy, and extracellular matrix remodeling. (Genome medicine, 2026, PMID 42152039): "...coupled dysregulation in lipid metabolism, mitophagy, and extracellular matrix remodeling."
Jun Lipid metabolism as a marker for glioma aggressiveness. (Bioscience reports, 2026, PMID 42144879): "Considering the important role of lipid metabolism in tumorigenesis, understanding the lipid-related pathways in glioma could lead to new important markers."
May Few-shot learning-driven discovery of Lutein suppresses Th1-mediated inflammation via glucose metabolism. (Acta pharmacologica Sinica, 2026, PMID 42144445): "...which targets PPARγ-mediated glucose metabolism to inhibit Th1 differentiation and ameliorate colitis."
May A comparison of deep multiomics profiles across ethnicity, geography, and age. (Cell, 2026, PMID 42134306): "Specific genetic variants and gene expression differences were associated with lipid metabolism and immune regulation."
May The acetylation status and metabolic characterization of the HBV-induced macrophages. (Journal of proteomics, 2026, PMID 41692303): "These findings suggest that HBV remodels macrophage acetylation and lipid metabolism, which may contribute to the development of an immunosuppressive microenvironment, providing new insights into potential therapeutic strategies targeting acetylation or lipid pathways in chronic HBV infection."