Cover Story Current Issue
Glucose is a ubiquitous and essential source of energy for all living organisms. Although mammals have evolved ways to convert other nutritional molecules to ATP, the preference for dietary glucose appears to be preserved. In rodents, the immediate detection of ingested glucose potently reinforces intake, hierarchically organizing behaviors towards glucose-yielding substances, and away from other types of food including other sugars. Taste is the primary sense linked to nutrient selection. Until recently, it was thought that most mammalian species utilize a single broadly tuned receptor to detect all simple sugars. Indeed, this “sweet” receptor, which comprises a heterodimer of the T1R2 and T1R3 proteins, binds multiple natural sugars (e.g., glucose, fructose, sucrose, maltose), as well as various other chemicals that yield little to no energy (e.g., low calorie sweeteners, sugar alcohols) and some d-amino acids. The neural signal originating from the sweet receptor is hardwired into brain circuits that drive eating and drinking behaviors, but it is an unreliable indicator of nutrient quality and quantity.
Current Issue
Protective role of soluble CD52 in obesity-associated steatotic liver disease and glucose dysregulation in mice
Protective role of soluble CD52 in obesity-associated steatotic liver disease and glucose dysregulation in mice
Objectives
Soluble CD52 (sCD52) derived from activated CD4+ T cells regulates T cell immunity under autoimmune conditions; however, its role in obesity-associated chronic inflammation and glucose metabolism remains unclear. Therefore, we herein investigated the significance of CD52 in obesity.
Methods
CD52-knockout mice (KO) and their wild-type littermates were fed a high-fat diet (HFD) for 12 weeks and analyzed.
Results
sCD52 preferentially suppressed chronic liver inflammation and protected against impaired glucose tolerance and metabolic dysfunction-associated steatotic liver disease (MASLD) in obesity. No significant differences were observed in weight gain or energy metabolism in KO mice; however, glucose metabolism was impaired. A histological examination revealed more severe chronic inflammation and steatosis in KO mice, accompanied by changes in liver transcriptome profiles, but no significant differences in epididymal white adipose tissue (eWAT). In contrast, CD52 expression was significantly up-regulated in eWAT, with slightly higher levels in the liver and skeletal muscle in HFD-fed obese C57BL/6 mice than in chow-fed controls. sCD52 was released from the cultured eWAT of obese mice, but not lean mice, and circulating sCD52 levels were higher in obese mice. A re-analysis of a public single-nucleus RNA sequencing library revealed that increased CD52 in eWAT was linked to immune cells and adipocytes. T cell-derived purified sCD52 suppressed macrophage activation in vitro. In contrast, sCD52 was not secreted from 3T3-L1 adipocytes, although its protein levels increased with differentiation.
Conclusions
T cell-derived sCD52 mitigates the obesity-associated development of MASLD and glucose intolerance in mice.
Articles in Press
Protective role of soluble CD52 in obesity-associated steatotic liver disease and glucose dysregulation in mice
Protective role of soluble CD52 in obesity-associated steatotic liver disease and glucose dysregulation in mice
Objectives
Soluble CD52 (sCD52) derived from activated CD4+ T cells regulates T cell immunity under autoimmune conditions; however, its role in obesity-associated chronic inflammation and glucose metabolism remains unclear. Therefore, we herein investigated the significance of CD52 in obesity.
Methods
CD52-knockout mice (KO) and their wild-type littermates were fed a high-fat diet (HFD) for 12 weeks and analyzed.
Results
sCD52 preferentially suppressed chronic liver inflammation and protected against impaired glucose tolerance and metabolic dysfunction-associated steatotic liver disease (MASLD) in obesity. No significant differences were observed in weight gain or energy metabolism in KO mice; however, glucose metabolism was impaired. A histological examination revealed more severe chronic inflammation and steatosis in KO mice, accompanied by changes in liver transcriptome profiles, but no significant differences in epididymal white adipose tissue (eWAT). In contrast, CD52 expression was significantly up-regulated in eWAT, with slightly higher levels in the liver and skeletal muscle in HFD-fed obese C57BL/6 mice than in chow-fed controls. sCD52 was released from the cultured eWAT of obese mice, but not lean mice, and circulating sCD52 levels were higher in obese mice. A re-analysis of a public single-nucleus RNA sequencing library revealed that increased CD52 in eWAT was linked to immune cells and adipocytes. T cell-derived purified sCD52 suppressed macrophage activation in vitro. In contrast, sCD52 was not secreted from 3T3-L1 adipocytes, although its protein levels increased with differentiation.
Conclusions
T cell-derived sCD52 mitigates the obesity-associated development of MASLD and glucose intolerance in mice.
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13th
Helmholtz Diabetes Conference
Munich, 21-23. Sep 2026
2024 impact factor: 6.6
You are what you eat
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