Diabetes & Metabolism Journal

Original Articles

Basic and Translational Research
Hepatocyte RAP1A Deletion Impairs Lipid Catabolism and Worsens Steatosis via Autophagy Activation: Xiujuan Wei, Yinxu Fu, Yu Fang, Xi Lin, Zhonggui Luo, Keyi Li, Kaiqiang Yang, Ting Fu, Liqin Jin, Jianxin Lyu, Qiongya Zhao; Received May 1, 2025 Accepted August 25, 2025 Published online November 24, 2025; DOI: https://doi.org/10.4093/dmj.2025.0388 [Epub ahead of print]

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Abstract PDF Supplementary Material PubReader ePub: Background
Metabolic disorders such as obesity, type 2 diabetes mellitus, and fatty liver disease are often linked to excessive hepatic lipid accumulation. This study aimed to determine the role of Ras-related protein 1a (RAP1A) in regulating hepatic lipid metabolism and to elucidate how RAP1A impacts metabolic dysfunction-associated fatty liver disease progression. We focused on RAP1A’s influence on liver lipid homeostasis and its connection to metabolic health.
Methods
A liver-specific Rap1a knockout (LKO) mouse model was generated and fed a high-fat diet to induce obesity and steatosis. Metabolic phenotyping (body weight, adiposity, glucose tolerance, insulin sensitivity) and liver analyses (histology, triglyceride/ cholesterol content, and gene expression profiling) were performed. In parallel, cultured hepatocyte models (alpha mouse liver 12 [AML12] cells) with RAP1A knockdown or overexpression were used to assess cellular lipid accumulation, fatty acid oxidation, and mechanistic pathways. Mitochondrial function assays, autophagy analysis, and extracellular signal-regulated kinase (ERK) signaling evaluations were conducted, including interventions with an ERK activator and autophagy inhibitor to probe pathway involvement.
Results
LKO mice developed increased adiposity and hepatic steatosis with significantly elevated liver triglycerides, cholesterol, and lipid droplet accumulation, despite unchanged caloric intake. They also exhibited impaired glucose tolerance and insulin resistance, indicating pronounced metabolic dysfunction. RAP1A deficiency led to dysregulated hepatic lipid gene expression—mainly downregulating genes for fatty acid oxidation and lipid catabolism—consistent with exacerbated lipid accumulation. Hepatocytes lacking RAP1A showed similar lipid accumulation, reduced fatty acid oxidation capacity, and altered expression of lipid metabolic enzymes. Mechanistically, RAP1A-deficient livers and cells displayed activated autophagy, particularly mitophagy. RAP1A was found to localize to mitochondrial membranes, and its loss was associated with reduced ERK phosphorylation. Notably, pharmacological activation of the ERK pathway restored ERK phosphorylation and significantly alleviated triglyceride accumulation in RAP1A-knockdown hepatocytes, rescuing the expression of key lipid breakdown enzymes. Conversely, inhibition of excessive autophagy in RAP1A-deficient cells also partially normalized lipid levels. These findings demonstrate that loss of RAP1A triggers hepatic lipid accumulation and metabolic dysregulation through coordinated effects on lipid metabolism genes, mitophagy, and ERK signaling.
Conclusion
RAP1A is a critical regulator of hepatic lipid metabolism, safeguarding against diet-induced steatosis and metabolic dysfunction. Its absence leads to lipid buildup and impaired metabolic homeostasis via disruptions in lipid accumulation, mitochondrial function, autophagy, and ERK signaling.

Others
Dynamic Lipidomic Remodeling and Clinical Correlations after Sleeve Gastrectomy in Obese Subjects: Gakyung Lee, Yeong Chan Lee, Minkuk Park, Seong Min Kim, Ji-Hyeon Park, Dae Ho Lee; Diabetes Metab J. 2026;50(2):396-411. Published online August 14, 2025; DOI: https://doi.org/10.4093/dmj.2025.0120

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Abstract PDF Supplementary Material PubReader ePub

Background
Sleeve gastrectomy (SG) is an effective and the most commonly performed surgical intervention for obesity. However, detailed studies on the underlying mechanisms, particularly those involving lipid metabolism, remain limited. This study aimed to identify novel pathways associated with the metabolic efficacy of SG by assessing alterations in the serum lipidomic profiles of obese subjects following surgery.
Methods
A prospective study of 50 obese participants undergoing laparoscopic SG was conducted at a tertiary medical center. Serum samples were collected before surgery and 6 months after SG. Lipidomic profiling was performed alongside comprehensive follow-up assessments. Statistical analyses explored lipidomic alterations and their correlations with changes in clinical parameters (Clinical trial registration No. KCT0003527 and KCT0009704).
Results
Participants experienced a 25% reduction in body weight 6 months after SG, with a marked reduction (>70%) in hepatic steatosis and insulin resistance, and a 2-fold increase in plasma oxyntomodulin levels. Lipidomic analysis revealed significant molecular shifts in lipid subclasses based on the fatty acyl composition of lipid species, showing a trend toward higher unsaturation and longer carbon chain lengths, as well as metabolic regulation in specific lipid pathways. Key findings included characteristic shifts within triacylglycerols and glycerophospholipids, which were significantly associated with changes in oxyntomodulin levels. Enhanced phosphatidylcholine-to-lysophosphatidylcholine conversion and upregulated ether lipid levels correlated with liver stiffness measures. Metabolic remodeling of sphingolipids—characterized by a decrease in ceramide/sphingomyelin levels and upregulation of the hexosylceramide pathway—emerged as an additional lipidomic signature after SG.
Conclusion
These findings highlight the complex lipidomic remodeling underlying the metabolic efficacy and therapeutic potential of SG.

Citations

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Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications
Xuan Trong Truong, Dae Ho Lee
Diabetes & Metabolism Journal.2025; 49(5): 964. CrossRef

Review

Metabolic Risk/Epidemiology
Glucagon-Like Peptide-1: New Regulator in Lipid Metabolism: Tong Bu, Ziyan Sun, Yi Pan, Xia Deng, Guoyue Yuan; Diabetes Metab J. 2024;48(3):354-372. Published online April 1, 2024; DOI: https://doi.org/10.4093/dmj.2023.0277

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Glucagon-like peptide-1 (GLP-1) is a 30-amino acid peptide hormone that is mainly expressed in the intestine and hypothalamus. In recent years, basic and clinical studies have shown that GLP-1 is closely related to lipid metabolism, and it can participate in lipid metabolism by inhibiting fat synthesis, promoting fat differentiation, enhancing cholesterol metabolism, and promoting adipose browning. GLP-1 plays a key role in the occurrence and development of metabolic diseases such as obesity, nonalcoholic fatty liver disease, and atherosclerosis by regulating lipid metabolism. It is expected to become a new target for the treatment of metabolic disorders. The effects of GLP-1 and dual agonists on lipid metabolism also provide a more complete treatment plan for metabolic diseases. This article reviews the recent research progress of GLP-1 in lipid metabolism.

Citations

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Original Articles

Metabolic Risk/Epidemiology
Biologically Informed Polygenic Scores for Brain Insulin Receptor Network Are Associated with Cardiometabolic Risk Markers and Diabetes in Women: Jannica S. Selenius, Patricia P. Silveira, Mikaela von Bonsdorff, Jari Lahti, Hannu Koistinen, Riitta Koistinen, Markku Seppälä, Johan G. Eriksson, Niko S. Wasenius; Diabetes Metab J. 2024;48(5):960-970. Published online March 25, 2024; DOI: https://doi.org/10.4093/dmj.2023.0039

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Background
To investigate associations between variations in the co-expression-based brain insulin receptor polygenic score and cardiometabolic risk factors and diabetes mellitus.
Methods
This cross-sectional study included 1,573 participants from the Helsinki Birth Cohort Study. Biologically informed expression-based polygenic risk scores for the insulin receptor gene network were calculated for the hippocampal (hePRS-IR) and the mesocorticolimbic (mePRS-IR) regions. Cardiometabolic markers included body composition, waist circumference, circulating lipids, insulin-like growth factor 1 (IGF-1), and insulin-like growth factor-binding protein 1 and 3 (IGFBP-1 and -3). Glucose and insulin levels were measured during a standardized 2-hour 75 g oral glucose tolerance test and impaired glucose regulation status was defined by the World Health Organization 2019 criteria. Analyzes were adjusted for population stratification, age, smoking, alcohol consumption, socioeconomic status, chronic diseases, birth weight, and leisure-time physical activity.
Results
Multinomial logistic regression indicated that one standard deviation increase in hePRS-IR was associated with increased risk of diabetes mellitus in all participants (adjusted relative risk ratio, 1.17; 95% confidence interval, 1.01 to 1.35). In women, higher hePRS-IR was associated with greater waist circumference and higher body fat percentage, levels of glucose, insulin, total cholesterol, low-density lipoprotein cholesterol, triglycerides, apolipoprotein B, insulin, and IGFBP-1 (all P≤0.02). The mePRS-IR was associated with decreased IGF-1 level in women (P=0.02). No associations were detected in men and studied outcomes.
Conclusion
hePRS-IR is associated with sex-specific differences in cardiometabolic risk factor profiles including impaired glucose regulation, abnormal metabolic markers, and unfavorable body composition in women.

Citations

Citations to this article as recorded by

A mesocorticolimbic insulin receptor gene co-expression network moderates the association between early life adversity and food approach eating behaviour style in childhood
Angela Marcela Jaramillo-Ospina, Roberta Dalle Molle, Sachin Patel, Shona Kelly, Irina Pokhvisneva, Carolina de Weerth, Patrícia Pelufo Silveira
Appetite.2025; 204: 107762. CrossRef
Early adversity and the comorbidity between metabolic disease and psychopathology
Ameyalli Gómez‐Ilescas, Patricia Pelufo Silveira
The Journal of Physiology.2025;[Epub] CrossRef
Brain insulin receptor gene network shapes risk for metabolic disease after early-life stress in women
Angela Marcela Jaramillo-Ospina, Guillaume Elgbeili, Sachin Patel, Irina Pokhvisneva, Patricia Pelufo Silveira
Communications Biology.2025;[Epub] CrossRef

Metabolic Risk/Epidemiology
Iron Overload and the Risk of Diabetes in the General Population: Results of the Chinese Health and Nutrition Survey Cohort Study: He Gao, Jinying Yang, Wenfei Pan, Min Yang; Diabetes Metab J. 2022;46(2):307-318. Published online March 7, 2022; DOI: https://doi.org/10.4093/dmj.2020.0287

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Abstract PDF Supplementary Material PubReader ePub

Background
Recent studies have found that there are significant associations between body iron status and the development of diabetes. In the present study, we aimed to analyze the association among iron overload (IO), insulin resistance (IR), and diabetes in Chinese adults, and to explore the sex difference.
Methods
Men and women (age >19 years) who participated in the Chinese Health and Nutrition Survey and did not have diabetes at baseline were followed between 2009 and 2015 (n=5,779). Over a mean of 6 years, 75 participants were diagnosed with incident diabetes. Logistic regression was used to assess the risk factors associated with IO. Cox proportional hazard regression was used to estimate the risk of incident diabetes and to determine whether the risk differed among subgroups. Causal mediation analysis (CMA) was used to explore the mechanism linking IO and diabetes.
Results
According to sex-stratified multivariable-adjusted Cox proportional hazards regression, IO increased the risk of incident diabetes. Women with IO had a higher risk of diabetes than men. Subgroup analysis with respect to age showed that the association between IO and diabetes was stronger in older women and younger men (P<0.001). CMA showed that liver injury (alanine transaminase) and lipid metabolism abnormalities (triglyceride, apolipoprotein B) contributed to the association between IO and diabetes.
Conclusion
IO is associated with diabetes and this association is sex-specific. IO may indirectly induce IR via liver injury and lipid metabolism abnormalities, resulting in diabetes.

Citations

Citations to this article as recorded by

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Effects of Smoking on Plasma Lipid Metabolism in Patients with non-insulin Dependent Diabetes Mellitus.: Seon Min Jeon, Yeun Kyung Lee, Hye Sung Lee, Bo Wan Kim, Young Bok Park, Myung Sook Choi; Korean Diabetes J. 1997;21(4):457-468. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Diabetes mellitus has been identified as a risk factor in the development of coronary vascular disease. Smoking also has been known as an independent risk factor in the development of coronary artery disease, causing a dislipidemia. This study was carried out to examine the effects of smoking on plasma lipids and lipoproteins metabolism in patients with NIDDM and in normal healthy subjects among Korean population in Taegu. METHODS: The 80 patients with NIDDM and 60 normal subjects were suMivided into non-stnoker, ex-smoker, and smoker group. Antbropornetric assessments, mean intake of nutrients, and the levels of plasma lipids, Apo A-I, L,p(a), CETP activity, and antioxidant vitamins such as vitamin A, E were measured, RESULTS: WHR in non-smoker of patients with NIDDM was greater than that in non-smoker of normal control. There were no differences in the nutrient intakes among groups, but protein intake was even higher in smoker of NIDDM group than that of normal group. There were no smoking effect on total cholesterol, LDL-C, AI, Apo A-I, Lp(a) and lipid peroxide in plasma of two groups, but they were higher in NIDDM group than normal group. Plasma TG concentrations were higher in smoker group than other groups within normal group, HDL-C levels were lower in non-smoker group than other groups within NIDDM group. CETP activities were higher in smoker group than non-smoker within normal group. And CEPT activities in NIDDM group were mostly higher than those of normal group. Vit. A levels of non-smoker in normal group were higher than ex-smoker within same group, and were also higher than non-smoker in NIDDM group. Vit. E levels showed no difference within each group, but they were mostly lower in NIDDM group than normal group. CONCLUSION: It was concluded that smoking was not a major factor for changing lipid metabolism in NIDDM patients as well as normal subjects unlike others findings. Their abnormal lipid rnetabolism may be induced from other risk factors for NIDDM rather than smoking itself. However, present study was done only for a short period, thus more studies are needed for longer term to investigate the effects af smoking on lipid metabolism in NIDDM among Korean population.

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