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Basic Research
Role of SUMO-Specific Protease 2 in Leptin-Induced Fatty Acid Metabolism in White Adipocytes
Praise Chanmee Kim, Ji Seon Lee, Sung Soo Chung, Kyong Soo Park
Diabetes Metab J. 2023;47(3):382-393.   Published online March 6, 2023
DOI: https://doi.org/10.4093/dmj.2022.0156
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  • 1 Web of Science
  • 1 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Leptin is a 16-kDa fat-derived hormone with a primary role in controlling adipose tissue levels. Leptin increases fatty acid oxidation (FAO) acutely through adenosine monophosphate-activated protein kinase (AMPK) and on delay through the SUMO-specific protease 2 (SENP2)–peroxisome proliferator-activated receptor δ/γ (PPARδ/γ) pathway in skeletal muscle. Leptin also directly increases FAO and decreases lipogenesis in adipocytes; however, the mechanism behind these effects remains unknown. Here, we investigated the role of SENP2 in the regulation of fatty acid metabolism by leptin in adipocytes and white adipose tissues.
Methods
The effects of leptin mediated by SENP2 on fatty acid metabolism were tested by siRNA-mediated knockdown in 3T3-L1 adipocytes. The role of SENP2 was confirmed in vivo using adipocyte-specific Senp2 knockout (Senp2-aKO) mice. We revealed the molecular mechanism involved in the leptin-induced transcriptional regulation of carnitine palmitoyl transferase 1b (Cpt1b) and long-chain acyl-coenzyme A synthetase 1 (Acsl1) using transfection/reporter assays and chromatin immunoprecipitation.
Results
SENP2 mediated the increased expression of FAO-associated enzymes, CPT1b and ACSL1, which peaked 24 hours after leptin treatment in adipocytes. In contrast, leptin stimulated FAO through AMPK during the initial several hours after treatment. In white adipose tissues, FAO and mRNA levels of Cpt1b and Acsl1 were increased by 2-fold 24 hours after leptin injection in control mice but not in Senp2-aKO mice. Leptin increased PPARα binding to the Cpt1b and Acsl1 promoters in adipocytes through SENP2.
Conclusion
These results suggest that the SENP2-PPARα pathway plays an important role in leptin-induced FAO in white adipocytes.

Citations

Citations to this article as recorded by  
  • Intermittent cold stimulation affects energy metabolism and improves stress resistance in broiler heart
    Tingting Li, Haidong Wei, Shijie Zhang, Xiaotao Liu, Lu Xing, Yuanyuan Liu, Rixin Gong, Jianhong Li
    Poultry Science.2024; 103(1): 103190.     CrossRef
Basic Research
Effects of Microbiota on the Treatment of Obesity with the Natural Product Celastrol in Rats
Weiyue Hu, Lingling Wang, Guizhen Du, Quanquan Guan, Tianyu Dong, Ling Song, Yankai Xia, Xinru Wang
Diabetes Metab J. 2020;44(5):747-763.   Published online May 11, 2020
DOI: https://doi.org/10.4093/dmj.2019.0124
  • 9,543 View
  • 140 Download
  • 16 Web of Science
  • 17 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background

Obesity has become one of the most serious issues threatening the health of humankind, and we conducted this study to examine whether and how celastrol protects against obesity.

Methods

We fed male Sprague-Dawley rats a high-fat diet and administered celastrol to obese rats for 3 weeks. By recording body weight (BW) and other measures, we identified the effective dose of celastrol for obesity treatment. Feces were collected to perform 16S rRNA sequencing, and hypothalami were extracted for transcriptome sequencing. We then treated leptin knockout rats with celastrol and explored the changes in energy metabolism. Male Institute of Cancer Research (ICR) mice were used to test the acute toxicity of celastrol.

Results

We observed that celastrol reduced BW and promoted energy expenditure at a dose of 500 µg/kg BW but that food intake was not changed after administration. The diversity of the gut microbiota was improved, with an increased ratio of Bacteroidetes to Firmicutes, and the gut microbiota played an important role in the anti-obesity effects of celastrol. Hypothalamic transcriptome analysis showed a significant enrichment of the leptin signaling pathway, and we found that celastrol significantly enhanced energy expenditure, which was mediated by the leptin signaling pathway. Acute lethal toxicity of celastrol was not observed at doses ranging from 0 to 62.5 mg/kg BW.

Conclusion

Our study revealed that celastrol decreased the BW of obese rats by enhancing energy expenditure but not by suppressing food intake and that this effect was mediated by the improvement of the gut microbiota and the activation of the hypothalamic leptin signaling pathway.

Citations

Citations to this article as recorded by  
  • Natural compounds as obesity pharmacotherapies
    Xin‐Yuan Zhao, Ji‐Qiu Wang, G. Gregory Neely, Yan‐Chuan Shi, Qiao‐Ping Wang
    Phytotherapy Research.2024; 38(2): 797.     CrossRef
  • Celastrol functions as an emerging manager of lipid metabolism: Mechanism and therapeutic potential
    Jia Gu, Ya-Ning Shi, Neng Zhu, Hong-Fang Li, Chan-Juan Zhang, Li Qin
    Biomedicine & Pharmacotherapy.2023; 164: 114981.     CrossRef
  • Tripterygium hypoglaucum extract ameliorates adjuvant-induced arthritis in mice through the gut microbiota
    Jianghui HU, Jimin NI, Junping ZHENG, Yanlei GUO, Yong YANG, Cheng YE, Xiongjie SUN, Hui XIA, Yanju LIU, Hongtao LIU
    Chinese Journal of Natural Medicines.2023; 21(10): 730.     CrossRef
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    Lili Su, Zhifan Hong, Tong Zhou, Yuanyuan Jian, Mei Xu, Xuanping Zhang, Xiaoyan Zhu, Jiayin Wang
    Scientific Reports.2022;[Epub]     CrossRef
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    Jiangping Wei, Liyun Chen, Sijia Gao, Jirui Wang, Yunhong Wang, Zhiwei Zhang, Yuyu Zhang, Xiaomei Zhang, Yong Yang, Dajian Yang
    Pharmacological Research - Modern Chinese Medicine.2022; 3: 100094.     CrossRef
  • Celastrol: An Update on Its Hepatoprotective Properties and the Linked Molecular Mechanisms
    Mengzhen Li, Faren Xie, Lu Wang, Guoxue Zhu, Lian-Wen Qi, Shujun Jiang
    Frontiers in Pharmacology.2022;[Epub]     CrossRef
  • Celastrol inhibits the proliferation and migration of MCF-7 cells through the leptin-triggered PI3K/AKT pathway
    Pingping Chen, Bin Wang, Meng Li, Chunxue Cui, Fei Liu, Yonggang Gao
    Computational and Structural Biotechnology Journal.2022; 20: 3173.     CrossRef
  • Investigating Celastrol’s Anti-DCM Targets and Mechanisms via Network Pharmacology and Experimental Validation
    Rui Xi, Yongxin Wan, Lihong Yang, Jingying Zhang, Liu Yang, Shuai Yang, Rui Chai, Fengchen Mu, Qiting Sun, Rui Yan, Zhifang Wu, Sijin Li, Zhijun Liao
    BioMed Research International.2022; 2022: 1.     CrossRef
  • Celastrol inhibits TXNIP expression to protect pancreatic β cells in diabetic mice
    Si-wei Wang, Tian Lan, Fang Zheng, Hui Huang, Hang-fei Chen, Qi Wu, Feng Zhang
    Phytomedicine.2022; 104: 154316.     CrossRef
  • Celastrol: A Promising Agent Fighting against Cardiovascular Diseases
    Zhexi Li, Jingyi Zhang, Xulei Duan, Guoan Zhao, Min Zhang
    Antioxidants.2022; 11(8): 1597.     CrossRef
  • Celastrol: A lead compound that inhibits SARS‐CoV‐2 replication, the activity of viral and human cysteine proteases, and virus‐induced IL‐6 secretion
    Carlos A. Fuzo, Ronaldo B. Martins, Thais F. C. Fraga‐Silva, Martin K. Amstalden, Thais Canassa De Leo, Juliano P. Souza, Thais M. Lima, Lucia H. Faccioli, Débora Noma Okamoto, Maria Aparecida Juliano, Suzelei C. França, Luiz Juliano, Vania L. D. Bonato,
    Drug Development Research.2022; 83(7): 1623.     CrossRef
  • In vitro activity of celastrol in combination with thymol against carbapenem-resistant Klebsiella pneumoniae isolates
    Mahmoud Saad Abdel-Halim, Momen Askoura, Basem Mansour, Galal Yahya, Amira M. El-Ganiny
    The Journal of Antibiotics.2022; 75(12): 679.     CrossRef
  • Celastrol alleviates metabolic disturbance in high‐fat diet‐induced obese mice through increasing energy expenditure by ameliorating metabolic inflammation
    Xueping Yang, Fan Wu, Lingli Li, Ernest C. Lynch, Linglin Xie, Yan Zhao, Ke Fang, Jingbin Li, Jinlong Luo, Lijun Xu, Xin Zou, Fuer Lu, Guang Chen
    Phytotherapy Research.2021; 35(1): 297.     CrossRef
  • Celastrol in metabolic diseases: Progress and application prospects
    Shaohua Xu, Yaqian Feng, Weishen He, Wen Xu, Wei Xu, Hongjun Yang, Xianyu Li
    Pharmacological Research.2021; 167: 105572.     CrossRef
  • The Anti-Obesity Effect of Traditional Chinese Medicine on Lipid Metabolism
    Qijing Fan, Furong Xu, Bin Liang, Xiaoju Zou
    Frontiers in Pharmacology.2021;[Epub]     CrossRef
  • Serum Metabolome Mediates the Antiobesity Effect of Celastrol-Induced Gut Microbial Alterations
    Shaohua Xu, Liwei Lyu, Huaichang Zhu, Xiaoqiang Huang, Wei Xu, Wen Xu, Yaqian Feng, Yong Fan
    Journal of Proteome Research.2021; 20(10): 4840.     CrossRef
  • Interrelated Mechanism by Which the Methide Quinone Celastrol, Obtained from the Roots of Tripterygium wilfordii, Inhibits Main Protease 3CLpro of COVID-19 and Acts as Superoxide Radical Scavenger
    Francesco Caruso, Manrose Singh, Stuart Belli, Molly Berinato, Miriam Rossi
    International Journal of Molecular Sciences.2020; 21(23): 9266.     CrossRef
Pathophysiology
Protective Effects of Ginger (Zingiber officinale) Extract against Diabetes-Induced Heart Abnormality in Rats
Behrouz Ilkhanizadeh, Alireza Shirpoor, Mohamad hasan Khadem Ansari, Samira Nemati, Yusef Rasmi
Diabetes Metab J. 2016;40(1):46-53.   Published online February 19, 2016
DOI: https://doi.org/10.4093/dmj.2016.40.1.46
  • 4,820 View
  • 71 Download
  • 34 Web of Science
  • 25 Crossref
AbstractAbstract PDFPubReader   
Background

Diabetic cardiomyopathy is an important causal factor in morbidity and mortality among diabetic patients, and currently, no effective means are available to reverse its pathological progress. The purpose of the present study was to investigate the effect of ginger extract on apolipoproteins (apo) A and B, hyperhomocysteinemia, cathepsin G and leptin changes, as well as cardiac fibrosis and heart muscle cell proliferation under hyperglycemic conditions in vivo.

Methods

Twenty-four male Wistar rats were divided into three groups, namely: control, non-treated diabetic, and ginger extract-treated diabetic groups. The ginger extract-treated diabetic group received a 50 mg daily dose of ginger extract intragastrically for 6 weeks.

Results

The results revealed concurrent significant increases in plasma C-reactive protein (CRP), homocysteine (Hcy), cathepsin G and apoB levels and decreases in apoA and leptin levels in the non-treated diabetic group compared to the control group. Moreover, heart structural changes, including fibrosis and heart muscle cell proliferation, were observed in non-treated diabetic rats compared to the control rats. Significant amelioration of changes in the heart structure together with restoration of the elevated levels of Hcy and CRP, leptin, cathepsin G, and apoA and B were found in the ginger extract-treated diabetic group compared to the non-treated diabetic group.

Conclusion

The findings indicated that ginger extract significantly reduces heart structural abnormalities in diabetic rats and that these effects might be associated with improvements in serum apo, leptin, cathepsin G, and Hcy levels and with the antioxidant properties of ginger extract.

Citations

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  • Cardioprotective Activities of some Indian Spices: An Insight into Pharmacology and Phytochemical Investigation
    Kalyani Pathak, Manash Pratim Pathak, Riya Saikia, Urvashee Gogoi, Jon Jyoti Sahariah, Aparoop Das, Mohammad Zaki Ahmad, Tirna Paul, Jyotirmoy Das, Saif Aboud M. Alqahtani
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    Maryam Maqsood, Saima Naaz, Huma Bader Ul Ain, Zunaira Mushtaq, Makia Nasir, Aiza Qamar
    Pakistan BioMedical Journal.2022; 5(1): 351.     CrossRef
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    Titin Sulastri, Marleen Sunyoto, Marvel Reuben Suwitono, Jutti Levita
    Journal Of Advanced Pharmacy Education And Research.2022; 12(3): 28.     CrossRef
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    Sadegh Shabab, Zahra Gholamnezhad, Maryam Mahmoudabady
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Relation of Absolute or Relative Adiposity to Insulin Resistance, Retinol Binding Protein-4, Leptin, and Adiponectin in Type 2 Diabetes
You Lim Kim, Tae Kyun Kim, Eun Sun Cheong, Dong Geum Shin, Gyu Sik Choi, Jihye Jung, Kyung-Ah Han, Kyung Wan Min
Diabetes Metab J. 2012;36(6):415-421.   Published online December 12, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.6.415
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  • 30 Download
  • 11 Crossref
AbstractAbstract PDFPubReader   
Background

Central fat mass (CFM) correlates with insulin resistance and increases the risk of type 2 diabetes and cardiovascular complications; however, peripheral fat mass (PFM) is associated with insulin sensitivity. The aim of this study was to investigate the relation of absolute and relative regional adiposity to insulin resistance index and adipokines in type 2 diabetes.

Methods

Total of 83 overweighted-Korean women with type 2 diabetes were enrolled, and rate constants for plasma glucose disappearance (KITT) and serum adipokines, such as retinol binding protein-4 (RBP4), leptin, and adiponectin, were measured. Using dual X-ray absorptiometry, trunk fat mass (in kilograms) was defined as CFM, sum of fat mass on the lower extremities (in kilograms) as PFM, and sum of CFM and PFM as total fat mass (TFM). PFM/TFM ratio, CFM/TFM ratio, and PFM/CFM ratio were defined as relative adiposity.

Results

Median age was 55.9 years, mean body mass index 27.2 kg/m2, and mean HbA1c level 7.12±0.84%. KITT was positively associated with PMF/TFM ratio, PMF/CFM ratio, and negatively with CFM/TFM ratio, but was not associated with TFM, PFM, or CFM. RBP4 levels also had a significant relationship with PMF/TFM ratio and PMF/CFM ratio. Adiponectin, leptin, and apolipoprotein A levels were related to absolute adiposity, while only adiponectin to relative adiposity. In correlation analysis, KITT in type 2 diabetes was positively related with HbA1c, fasting glucose, RBP4, and free fatty acid.

Conclusion

These results suggest that increased relative amount of peripheral fat mass may aggravate insulin resistance in type 2 diabetes.

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Reviews
Molecular Mechanisms of Appetite Regulation
Ji Hee Yu, Min-Seon Kim
Diabetes Metab J. 2012;36(6):391-398.   Published online December 12, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.6.391
  • 9,292 View
  • 229 Download
  • 81 Crossref
AbstractAbstract PDFPubReader   

The prevalence of obesity has been rapidly increasing worldwide over the last several decades and has become a major health problem in developed countries. The brain, especially the hypothalamus, plays a key role in the control of food intake by sensing metabolic signals from peripheral organs and modulating feeding behaviors. To accomplish these important roles, the hypothalamus communicates with other brain areas such as the brainstem and reward-related limbic pathways. The adipocyte-derived hormone leptin and pancreatic β-cell-derived insulin inform adiposity to the hypothalamus. Gut hormones such as cholecystokinin, peptide YY, pancreatic polypeptide, glucagon-like peptide 1, and oxyntomodulin transfer satiety signals to the brain and ghrelin relays hunger signals. The endocannabinoid system and nutrients are also involved in the physiological regulation of food intake. In this article, we briefly review physiological mechanisms of appetite regulation.

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Leptin in Relation to the Lipodystrophy-Associated Metabolic Syndrome
Christos S. Mantzoros
Diabetes Metab J. 2012;36(3):181-189.   Published online June 14, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.3.181
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AbstractAbstract PDFPubReader   

Leptin, an adipocyte-secreted hormone, regulates energy homeostasis as well as reproductive, neuroendocrine, immune and metabolic functions. Subjects with decreased amounts of fat in their adipose tissue, i.e., lipoatrophy, have low leptin levels. In the context of open-label, uncontrolled studies leptin administration, in physiological replacement doses, has been shown to have metabolically salutary effects in the rare patients with the syndrome of congenital lipodystrophy accompanied by leptin deficiency. Much more patients with lipodystrophy suffer from lipodystrophy and the metabolic syndrome associated with the use of highly active antiretroviral therapy. In this so called highly active antiretroviral therapy (HAART)-associated lipodystrophy and metabolic syndrome, patients demonstrate fat maldistribution with dyslipidemia, insulin resistance, and other metabolic complications. Leptin administration has been shown to decrease central fat mass and to improve fasting insulin/glucose levels and insulin sensitivity in human immunodeficiency virus-infected hypoleptinemic patients with HAART induced lipodystrophy and the metabolic syndrome. By contrast, the results of leptin treatment in leptin replete or hyperleptinemic obese individuals with glucose intolerance and diabetes mellitus have been minimal or null, presumably due to leptin tolerance or resistance that impairs leptin action. In this review, we present the emerging clinical applications and potential therapeutic uses of leptin in humans with lipodystrophy and the metabolic syndrome.

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Original Articles
The Relationship of Adiponectin/Leptin Ratio with Homeostasis Model Assessment Insulin Resistance Index and Metabolic Syndrome in Apparently Healthy Korean Male Adults
Chan-Hee Jung, Eun-Jung Rhee, Ji-Hoon Choi, Ji-Cheol Bae, Seung-Hyun Yoo, Won-Jun Kim, Cheol-Young Park, Ji Oh Mok, Chul Hee Kim, Won-Young Lee, Ki-Won Oh, Sung-Woo Park, Sun-Woo Kim
Korean Diabetes J. 2010;34(4):237-243.   Published online August 31, 2010
DOI: https://doi.org/10.4093/kdj.2010.34.4.237
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AbstractAbstract PDFPubReader   
Background

We investigated the relationships of adiponectin/leptin (A/L) ratio with cardiovascular risk factors, insulin resistance index, and metabolic syndrome (MS) in apparently healthy Korean male adults.

Methods

Sixty-eight male subjects were enrolled among the participants of an annual health check-up program (mean age, 55.1 years). Percent body fat (%) was measured using a bioelectric impedance analyzer. Serum leptin level was measured via radioimmunoassay, and adiponectin level was measured using an enzyme-linked immunosorbent assay. Homeostasis model assessment (HOMA)-insulin resistance (IR) index was calculated, and the presence of metabolic syndrome was assessed.

Results

Adiponectin, leptin, and A/L ratio showed significant correlations with percent body fat, lipid profile, and HOMA-IR. Mean leptin and HOMA-IR levels were significantly higher, while A/L ratio was significantly lower in subjects with MS. With increasing number of MS components, the mean values of leptin and HOMA-IR increased and the A/L ratio decreased. In multiple regression analysis, HOMA-IR was significantly correlated with triglyceride, fasting glucose, and A/L ratio, while A/L ratio was significantly correlated with body mass index and HOMA-IR. HOMA-IR and A/L ratio were significant predictors for each other after adjustment for other factors.

Conclusion

A/L ratio correlated well with lipid profile, HOMA-IR, and the presence and number of MS components in Korean male subjects.

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Leptin is Negatively Associated with Femoral Bone Mineral Density in Postmenopausal Women with Type 2 Diabetes Mellitus.
Jae Han Jeon, Yeun Kyung Choi, Hyun Ae Seo, Jung Eun Lee, Ji Yun Jeong, Seong Su Moon, Ju Young Lee, Jung Guk Kim, Bo Wan Kim, In Kyu Lee
Korean Diabetes J. 2009;33(5):421-431.   Published online October 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.5.421
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AbstractAbstract PDF
BACKGROUND
Serum leptin level and bone mineral density (BMD) are widely assumed to be positively associated with body fat mass. Numerous attempts have been made to document the relationship between leptin and BMD, but the results are inconsistent, especially in diabetic patients. METHODS: A total of 60 Korean postmenopausal women with type 2 diabetes mellitus were included in the present study. The BMDs of lumbar spines (L1 to L4) and proximal femurs (trochanter, neck, and total) were measured by dual-energy X-ray absorptiometry (DXA), and biochemical markers including leptin, HbA1c, C-peptide and urine albumin-creatinine ratio (ACR) were measured for each patient. RESULTS: Negative associations between leptin and BMD of femoral neck, trochanter, and total femur in postmenopausal women with type 2 diabetes mellitus were documented in a model adjusted for age, body fat mass, and fasting insulin level (r = -0.308, P = 0.020 and r = - 0.303, P = 0.025 and r = - 0.290, P = 0.032 respectively). Multiple linear regression analysis was performed revealing negative associations between leptin and BMD of the femoral neck (beta = -0.369), trochanter (beta = -0.324), and total femur (beta = -0.317). CONCLUSION: The results of the present study suggest a negative relationship between leptin and femoral BMD. In addition, leptin may have a negative effect on BMD in postmenopausal women with type 2 diabetes mellitus.

Citations

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  • Evaluation of bone mineral density in type 2 diabetes mellitus patients before and after treatment
    MK Dutta, R Pakhetra, MK Garg
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The Role of Hypothalamic FoxO1 on Hyperphagia in Streptozotocin-Induced Diabetic Mice.
Il Seong Nam-Goong, Jae Geun Kim, Se Jin Kim, Seong Jae Hur, Jin Woo Lee, Eun Sook Kim, Chang Ho Yun, Byung Ju Lee, Young Il Kim
Korean Diabetes J. 2009;33(5):375-381.   Published online October 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.5.375
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AbstractAbstract PDF
BACKGROUND
Streptozotocin-induced diabetic animals are characterized by hyperphagia due to deficiencies of insulin and leptin. Forkhead box-containing protein of the O subfamily-1 (FoxO1) regulates energy homeostasis by regulating energy expenditure and food intake as well as mediating insulin and leptin signals in the hypothalamus. To identify the mediator of diabetic hyperphagia, we examined the effects of insulin or leptin on hypothalamic FoxO1 expression in a diabetic animal model. METHODS: Diabetes was induced in mice (C57BL/6) by intraperitoneal administration of streptozotocin (200 mg/kg). Stainless steel cannula was implanted into the lateral ventricle of the brain in each mouse. After three weeks, the mice were administered saline, insulin or leptin via intracerebroventricular (ICV) route. The medial hypothalamus was isolated to evaluate the mRNA expressions of FoxO1 and neuropeptides. RESULTS: Streptozotocin-induced diabetic mice exhibited significant elevations of blood glucose and food intake and significantly low levels of serum insulin and leptin. The levels of hypothalamic FoxO1 mRNA were significantly increased in diabetic mice. The hypothalamic expression of neuropeptide Y (NPY) mRNA was increased, but the expression of preproopiomelanocortin (POMC) mRNA was decreased in diabetic mice. ICV administration of insulin or leptin attenuated the upregulation of hypothalamic FoxO1 mRNA, and resulted in downregulation of NPY mRNA and upregulation of POMC mRNA in diabetic mice. CONCLUSION: We observed that the expression of hypothalamic FoxO1 mRNA was increased in streptozotocin-induced diabetic mice, and that it was significantly attenuated by central administration of insulin or leptin. These results suggest that hypothalamic FoxO1 is the direct mediator of diabetic hyperphagia.
Adipokine Concentrations in Pregnant Korean Women with Normal Glucose Tolerance and Gestational Diabetes Mellitus.
Eun Suk Oh, Jung Hee Han, Sung Min Han, Jee Aee Im, Eun Jung Rhee, Cheol Young Park, Ki Won Oh, Won Young Lee
Korean Diabetes J. 2009;33(4):279-288.   Published online August 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.4.279
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AbstractAbstract PDF
BACKGROUND
The aims of this study were to compare adipokine concentrations of pregnant women in the 24th~28th weeks of gestation to those of non-pregnant women. We compared the concentrations of adipokines in women with gestational diabetes mellitus (GDM), gestational impaired glucose tolerance (GIGT) and normal glucose tolerance (NGT). We also investigated the role of adipokines in the development of gestational glucose intolerance. METHODS: We surveyed 129 pregnant women who underwent a 100 g oral glucose tolerance test (OGTT) during the 24th~28th weeks of gestation. Participants were classified into three groups: (1) NGT (n = 40), (2) GIGT (n = 45), and (3) GDM (n = 44). Pregnant subjects with NGT were matched to non-pregnant controls for BMI and age (n = 41). RESULTS: Pregnant women with NGT exhibited significantly decreased adiponectin levels and elevated leptin levels compared to non-pregnant controls. Mean plasma resistin levels were significantly higher in women with GDM and GIGT than in women with NGT. Resistin and fasting glucose were significant predictors for the development of gestational glucose intolerance. CONCLUSION: Plasma adiponectin levels were decreased and leptin levels were increased in pregnant subjects with NGT compared to BMI and age matched non-pregnant controls. Women with GDM and GIGT exhibit significantly elevated concentrations of resistin compared with women with NGT. Increased resistin levels were also associated with the development of gestational glucose intolerance. Resistin may play an important role on the development of gestational glucose intolerance in Korean women.

Citations

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  • Maternal serum level of resistin is associated with risk for gestational diabetes mellitus: A meta-analysis
    Shi-Min Hu, Meng-Shi Chen, Hong-Zhuan Tan
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  • Letter: Adipokines and Insulin Resistance According to Characteristics of Pregnant Women with Gestational Diabetes Mellitus (Diabetes Metab J 2017;41:457-65)
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  • Adipokines and Insulin Resistance According to Characteristics of Pregnant Women with Gestational Diabetes Mellitus
    Eon Ju Jeon, Seong Yeon Hong, Ji Hyun Lee
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Blood Leptin, Anthropometric and Biochemical Parameters in Type 2 Diabetics.
Seong su Moon, Jae han Jeon, Jung eun Lee, Soon hong Park, Hee kyung Kim, Jeong yun Doh, Ye dal Jung, In kyu Lee, Bo wan Kim, Jung guk Kim
Korean Diabetes J. 2007;31(1):75-82.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.75
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AbstractAbstract PDF
BACKGROUND
Leptin is a hormone which is produced in adipose tissue and regulates food intake and body weight. Leptin is known to correlate with body adiposity such as body mass index. Blood leptin concentration is not different between non-diabetics and diabetics. And It affect not only food intake but may be one of the key factors in the developement of insulin resistance. Recent studies suggest a complex relationship between leptin and insulin resistance or insulin. Therefore we examined the relationship between leptin and anthropometric, biochemical parameters, and insulin resistance in type 2 diabetics. METHOD: The study subjects were 144 patients with type 2 diabetes who visited Kyungpook national university hospital. Anthropometric parameters such as body fat mass, soft lean mass, BMI, arm circumference, skin fold thickness of several sites were measured. Percent body fat were calculated from Brozek fomula, body density were calculated from Jackson and Pollock fomula. Fasting blood leptin and metabolic varables such as C-peptide, HbA1C, insulin, HDL, LDL, TG, total cholesterol, FFA, HOMA-IR were measured. The relationships of blood leptin concentration with clinical data were analyzed with SPSS program. RESULT: Blood leptin concentrations were 8.2 +/- 5.39 ng/mL in women with type 2 diabetes and 5.1 +/- 5.55 ng/mL in men with type 2 diabetes (P-value: 0.01). Percent body fat, FFA were higher in women than men but arm circumference, soft lean mass, waist circumference were higher in men than women (P-value < 0.05). Leptin concentration correlated with BMI, percent body fat, insulin, TG, body fat mass, waist circumference, HOMA-IR. And insulin, C-peptide, total cholesterol, TG were also correlated with leptin only in women with type 2 diabetes. Waist circumference and percent body fat were independent variables which influence blood leptin concentration in multiple regression analysis. CONCLUSION: Blood leptin concentrations are related to parameters such as percent body fat, waist circumference, BMI, body fat mass, insulin, TG, HOMA-IR in type 2 diabetics. The relationship between leptin and obesity or HOMA-IR suggests that leptin may be a one of factors in developement of insulin resistance.

Citations

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  • Prognostic Value of Leptin in Terminally Ill Cancer Patients
    Ji Hyun Hong, So Jin Lee, Sang Mi Kwak, Youn Seon Choi, June Yeong Lee
    The Korean Journal of Hospice and Palliative Care.2012; 15(2): 99.     CrossRef
Comparison of the Relationship of Leptin to Metabolic Parameters Between Premenopausal Normal Weight and Obese Women.
Hee Kyoung Kim, Keun Gyu Park, Mi Kyung Kim, Young Yun Jang, Sang Yoon Kim, Eui Dal Jung, Hye Soo Kim, Ju Ho Do, In Kyu Lee
Korean Diabetes J. 2005;29(3):223-230.   Published online May 1, 2005
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AbstractAbstract PDF
BACKGROUND
Leptin is mainly secreted from adipose tissue, and it is a crucial factor for metabolic syndrome that is characterized by obesity, insulin resistance, hypertension and dyslipidemia. We measured the serum leptin concentrations and compared them with the body fat distribution and metabolic risk factors in premenopausal normal weight and obese women. METHODS: 231 premenopausal obese women participated in this study. The subjects were grouped based on their body mass index(BMI). The number of normal weight group women(BMI<25kg/m2) and the number of obese group women(BMI> or = 25kg/m2) were 90 and 141, respectively. We measured the plasma leptin concentration and such metabolic risk factors as fasting glucose, insulin, triglyceride(TG), systolic blood pressure(SBP) and diastolic blood pressure(DBP). The subcutaneous adipose tissue area(SAT) and the visceral adipose tissue area(VAT) were determined by computed tomography. The BMI, waist to hip ratio(WHR) and homeostasis model assessment(HOMA-IR) were calculated. RESULTS: In the obese group, the leptin levels were positively correlated with the BMI and SAT as well as with such metabolic risk factors as fasting serum glucose, insulin, HOMA-IR, TG, SBP and DBP. Although leptin levels were positively correlated with BMI and SAT in the normal weight group, they were not correlated with the metabolic risk factors. CONCLUSION: The present study showed that the leptin levels in the normal weight group were not associated with the metabolic risk factors. Therefore, the degree of obesity must be considered before leptin can be used as a predictor for metabolic syndrome including diabetes and coronary heart disease
Randomized Controlled Trial
The Effects of Insulin Sensitizers on the Plasma Concentrations of Adipokines in Type 2 Diabetic Patients.
Hye Seung Jung, Young Min Cho, Kyung Won Kim, Byung Soo Youn, Kang Yeol Yu, Hong Je Park, Chan Soo Shin, Seong Yeon Kim, Hong Kyu Lee, Kyong Soo Park
Korean Diabetes J. 2003;27(6):476-489.   Published online December 1, 2003
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AbstractAbstract PDF
BACKGROUND
Resistin, leptin and adiponectin are proteins secreted from adipose tissue, and have been suggested to play roles in insulin sensitivity. The effects of the circulating levels of two different types of insulin sensitizer, rosiglitazone and metformin, in type 2 diabetic patients were examined to elucidate the relationship between adipokines and insulin resistance. METHODS: Thirty type 2 diabetic patients, who showed poor glycemic control when administered 4 mg glimepiride a day, without severe diabetic complications or medical illness, were randomized to receive an additional 4mg rosiglitazone or 1000 mg metformin a day. The plasma resistin, leptin and adiponectin concentrations were measured at the baseline and after 6 months of treatment. The anthropometric parameters, fasting plasma glucose, HbA1C, total cholesterol, triglyceride, HDL-cholesterol and free fatty acids were also measured. Certain single nucleotide polymorphisms of adipokine genes were also identified. RESULTS: There were no significant differences in the reductions of the plasma glucose and HbA1C levels, after 6 months of treatment, between the two groups. The plasma resistin concentrations decreased, the adiponectin significantly increased and the leptin showed a tendency to increase in the rosiglitazone group. In the metformin group, only the resistin concentration significantly increased. However, the changes in the adipokines did not correlate with the HOMA-IR in either group. The reduction in the HbA1C due to rosiglitazone was greater if the initial leptin level was high, if there was a G allele on the -420th locus of the resistin gene, or the 45th locus of the APM1 (adiponectin gene) was the T-homozygote or there was a T allele on the 276th locus of the APM1. Those due to metfromin were greater with high initial adiponectin levels. CONCLUSION: In type 2 diabetic patients, showing poor glycemic control with sulfonylurea therapy, rosiglitazone or metformin treatment changed some of the adipokine concentrations, but these changes were not clearly related with insulin resistance. Polymorphisms of certain adipokine genes seem to have a relation to the susceptibility of rosiglitazone.
Original Articles
Efficacy of Serum Leptin Level as an Indicator to Predict the Clinical Response of Rosiglitazone in Patients with Type 2 Diabetes Mellitus.
Jae Hyuk Lee, Soo Kyung Kim, Kyu Yeon Hur, Han Seok Choi, Ji Young Jung, Wan Sub Shim, Hyun Joo Lee, Chul Woo Ahn, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Bong Soo Cha
Korean Diabetes J. 2003;27(5):420-432.   Published online October 1, 2003
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AbstractAbstract PDF
BACKGROUND
Leptin is a protein secreted by adipocytes that regulates food intake by acting on the hypothalamus and is correlated with body fat mass. Insulin resistance is also correlated with body fat mass and obesity. Rosiglitazone (RSG) is known as a highly selective and potent agonist for the peroxisome proliferator-activated receptor-gamma (PPARgamma). It improves glycemic control by improving insulin sensitivity in peripheral tissue. This study was performed to evaluate the antidiabetic and insulin sensitizing effects of RSG combination therapy and the efficacy of serum leptin level as an indicator to predict the clinical response of RSG in type 2 diabetic patients with oral agents such as metformin and/or sulfonylurea. METHODS: The study subjects were 140 type 2 diabetic patients (90 male, 50 female) who received a 12-week course of daily 4 mg RSG, in addition to the previous medications. The glucose level, indices of insulin resistance and metabolic parameters were measured. Serum leptin level was measured by radioimmunoassay before and after RSG treatment. Visceral fat and subcutaneous fat were measured by sonography. RESULTS: After 12 weeks of RSG treatment, FPG (12.6+/-28.1 mg/dL), HOMAIR (0.3+/-0.9), serum fasting insulin (1.9+/-4.7 microU/mL), SBP and DBP had all decreased significantly, whereas body weight, BMI, waist circumference, WHR, body fat mass, and subcutaneous fat had all increased. Serum leptin level also tended to increase after RSG treatment, but without significance. deltaFPG (delta=value after treatment- value before treatent) was inversely correlated with basal serum leptin level (r=-0.202), basal HOMAIR (r=-0.226) and basal FPG (r=-0.565). There was no correlation between deltaFPG and basal BMI or serum insulin level. RSG treatment showed significant inverse correlation between serum leptin level and deltaHOMAIR (r=-0.416), delta insulin (r=-0.365) and deltaHbA1c (r=-0.189). Serum leptin level was positively correlated with the subcutaneous fat amount (r=0.548), basal BMI (r=0.521), and basal HOMAIR (r=0.343). CONCLUSION: These results showed that RSG treatment can improve not only hyperglycemia but also insulin resistance in type 2 diabetic patients. The serum leptin level at baseline can be used as an indicator to predict the clinical response of RSG treatment in type 2 diabetes patients.
Association between Hyperleptinemia and Metabolic Syndrome in an Urban Korean Community.
Jee Young Oh, Young Sun Hong, Yeon Ah Sung
Korean Diabetes J. 2003;27(4):313-322.   Published online August 1, 2003
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AbstractAbstract PDF
BACKGROUND
To determine whether hyperleptinemia is a principal component of metabolic syndrome in a Korean population using factor analysis. METHODS: Metabolic syndrome was defined by the NCEP-ATP III guideline. An oral glucose tolerance test was performed, and plasma samples for leptin and lipid profiles were collected from 199 men and 426 women who had no history of diabetes, hypertension, dyslipidemia, or of taking lipid-lowering, antihypertensive, or antihyperglycemic medications. RESULTS: Leptin level was correlated with overall and central obesity, blood pressure, and glucose or insulin levels in men and women aged 30 to 83. Before and after adjustment for BMI, leptin level was significantly and positively correlated, in women only, with insulin and with insulin resistance, as assessed by a homeostasis model assessment (HOMA) (Ps<0.0001). Factor analysis identified the following four factors from among the metabolic syndrome variables; an obesity/hyperinsulinemia factor, a glucose intolerance factor, a hypertension factor, and a dyslipidemia factor in men. Leptin was clustered as an obesity/ hyperinsulinemia and a dyslipidemia factor in men. In women, four different groups were found: an obesity/hypertension factor, a glucose intolerance factor, an obesity/dyslipidemia factor, and an obesity/hyperinsulinemia factor. Leptin was clustered as an obesity/hyperinsulinemia factor in women. CONCLUSION: Our research suggests that leptin level is associated with metabolic syndrome in relation to obesity and hyperinsulinemia. Moreover, obesity, as opposed to hyperinsulinemia, is related to hypertension or dyslipidemia in women only, and this gender differences may reflect different roles of central adiposity on metabolic abnormalities.

Diabetes Metab J : Diabetes & Metabolism Journal