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.
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Diabetes Metab J. 2024;48(5):960-970. Published online March 25, 2024
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.
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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.
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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.