Leptin: A new therapeutic target for treatment of diabetes mellitus

Rehman, Kanwal; Akash, Muhammad Sajid Hamid; Alina, Zunaira

doi:10.1002/jcb.26580

Cited by 35 publications

(29 citation statements)

References 81 publications

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“…During leptin resistance, there is an increased secretion of leptin from white adipose tissue, but this leptin does not bind with its receptor (LEP-R) present on hypothalamus in brain, causing resistance to the leptin and increasing the body weight which leads to the obesity [1]. Various factors are considered responsible for this unavoidable condition of hyperleptinemia [45]; likewise, different conventional drugs are being used for its management including inhibitor of pancreatic lipase, like orlistat. This drug may act to decrease the body weight by reducing the absorption of fat [46].…”

Section: Discussionmentioning

confidence: 99%

Hesperidin improves insulin resistance via down-regulation of inflammatory responses: Biochemical analysis and in silico validation

et al. 2020

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Leptin resistance and co-existing insulin resistance is considered as hallmark of dietinduced obesity. Here, we investigated therapeutic potential of hesperidin to improve leptin and insulin resistance using high fat diet (HFD)-induced obese experimental animal model. We also performed in silico studies to validate therapeutic effectiveness of hesperidin by performing protein-ligand docking and molecular dynamics simulation studies. Group 1 was identified as control group receiving vehicle only. Group 2 was marked as non-treated group receiving 60% HFD. While, other groups were treated daily with orlistat (120 mg/kg/d), hesperidin (55 mg/kg/d), combination of hesperidin (55 mg/kg/d) + orlistat (120 mg/kg/d). Hesperidin alone (P<0.001) and particularly in combination with orlistat (P<0.001), resulted in controlling the levels of HFD-altered biomarkers including random and fasting state of glycemia, leptin and insulin resistance. Similarly, hesperidin also improved the serum and tissue levels of leptin, interleukin-6 and tumor necrosis factor-alpha more significantly (P<0.05) when compared with that of orlistat. These results were found to be in accordance with the results of histopathological examination of pancreas, liver and adipose tissues. In-silico studies also proved that hesperidin binds to leptin receptor with higher affinity as compared to that of orlistat and induces the favorable variations in geometrical conformation of leptin receptor to promote its association with leptin which may lead to the cascades of reactions culminating the lipolysis of fats that may ultimately lead to cure obesity. The results of this study may be a significant expectation among the forthcoming treatment strategies for leptin and insulin resistance.

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Section: Discussionmentioning

confidence: 99%

Hesperidin improves insulin resistance via down-regulation of inflammatory responses: Biochemical analysis and in silico validation

et al. 2020

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“…LEP is a protein product encoded by the OB gene and synthesized by the adipocytes. It regulates blood sugar by inhibiting insulin secretion, and is closely related to obesity, dyslipidemia, insulin resistance and associated conditions [27].…”

Section: Discussionmentioning

confidence: 99%

Correlation of serum 25-hydroxy vitamin D with Leptin and visceral fat area in T2DM patients combined with osteoporosis

Wang¹,

Wang²,

Wei³

et al. 2019

biomedicalresearch

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Purpose: To investigate the correlation of serum 25-hydroxy vitamin D [25(OH)D] with leptin (LEP) and visceral fat area (VFA) in type 2 diabetes mellitus (T2DM) patients with osteoporosis (OP). Methods: A total of 135 T2DM patients with newly diagnosed admitted to the Department of Endocrinology, Affiliated Hospital of Zunyi Medical College. The patients were divided into three groups according to BMD status: (1) DMNB group, n=45; (2) DMLB group, n=45; and (3) DMOP group, n=45. The control group consisted of 50 age and gender matched subjects recruited from the Physical Examination Center (NC group). All patients were examined for general biochemical indicators and QCT was used to measure VFA. Electrochemiluminescence (ECL) and enzyme linked immunosorbent assay (ELISA) were used to evaluate the serum levels of 25 (OH)D and LEP, respectively. Results: Compared with NC group, the levels of 25 (OH)D, L1-L4 lumbar vertebrae and left femoral neck BMD in DMNB group, DMLB group and DMOP group were significantly lower (P<0.05), the LEP and VFA levels were significantly increased (P<0.05). Conclusions: Our data showed a strong correlation between decreased 25 (OH)D and increased LEP serum levels in T2DM patients presenting with comorbid OP. This patient cohort also exhibited significantly higher VFA, which is symptomatic of imbalanced glucose and lipid metabolism.

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“…Similar to adipose tissue, the stomach simultaneously expresses leptin and ObR. Leptin maintains energy homeostasis with the aid of its antagonistic hormone ghrelin [190]. Ghrelin is a gut-derived peptide hormone that was first isolated from the stomach [191].…”

Section: Leptinmentioning

confidence: 99%

Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression

Chang

Yang

2020

IJMS

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Adipose tissue is a highly dynamic endocrine tissue and constitutes a central node in the interorgan crosstalk network through adipokines, which cause pleiotropic effects, including the modulation of angiogenesis, metabolism, and inflammation. Specifically, digestive cancers grow anatomically near adipose tissue. During their interaction with cancer cells, adipocytes are reprogrammed into cancer-associated adipocytes and secrete adipokines to affect tumor cells. Moreover, the liver is the central metabolic hub. Adipose tissue and the liver cooperatively regulate whole-body energy homeostasis via adipokines. Obesity, the excessive accumulation of adipose tissue due to hyperplasia and hypertrophy, is currently considered a global epidemic and is related to low-grade systemic inflammation characterized by altered adipokine regulation. Obesity-related digestive diseases, including gastroesophageal reflux disease, Barrett’s esophagus, esophageal cancer, colon polyps and cancer, non-alcoholic fatty liver disease, viral hepatitis-related diseases, cholelithiasis, gallbladder cancer, cholangiocarcinoma, pancreatic cancer, and diabetes, might cause specific alterations in adipokine profiles. These patterns and associated bases potentially contribute to the identification of prognostic biomarkers and therapeutic approaches for the associated digestive diseases. This review highlights important findings about altered adipokine profiles relevant to digestive diseases, including hepatic, pancreatic, gastrointestinal, and biliary tract diseases, with a perspective on clinical implications and mechanistic explorations.

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Leptin: A new therapeutic target for treatment of diabetes mellitus

Cited by 35 publications

References 81 publications

Hesperidin improves insulin resistance via down-regulation of inflammatory responses: Biochemical analysis and in silico validation

Hesperidin improves insulin resistance via down-regulation of inflammatory responses: Biochemical analysis and in silico validation

Correlation of serum 25-hydroxy vitamin D with Leptin and visceral fat area in T2DM patients combined with osteoporosis

Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression

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