Leptin, cardiovascular diseases and type 2 diabetes mellitus

Katsiki, Niki; Mikhailidis, Dimitri P.; Banach, Maciej

doi:10.1038/aps.2018.40

Cited by 236 publications

(183 citation statements)

References 212 publications

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“…Leptin, a vital hormone derived from adipose tissue, plays a significant role in various pathways prompting the risk of diabetes and cardiovascular diseases (Patel et al, 2016;Katsiki et al, 2018). In current study, diabetes induction by alloxan significantly increased (P≤0.05) leptin concentration in serum, while a significant decrease in serum leptin level (P≤0.05) was observed in high protein diet group.…”

Section: Discussionsupporting

confidence: 45%

High Protein Diet Improves Biochemical and Metabolic Hormonal Profile in Alloxan-Induced Diabetic Rats

Muzaffar¹

2019

PVJ

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Diabetes mellitus is a metabolic disorder characterized by high blood glucose level due to defective insulin secretion or action and is considered one of the major concerns to human health all over the world. Current study was planned to assess the effects of protein rich diet on body weight, glycemic control, insulin levels in hyperglycemic rats. For this purpose, high protein diet (45% or 55% fish protein rich in omega 3 fatty acids) was administered to alloxan-induced diabetic rats for a period of 28 days. Blood samples were collected for monitoring glucose level, serum insulin level and thyroid hormone levels. Alloxan administration resulted in reduced body weight, increased blood glucose, leptin while decreased insulin, amylin, glucokinase, thyroid stimulating hormone (TSH), triiodothyronin (T3) and thyroxin (T4) levels. High protein diet significantly restored body weight and showed significant anti-diabetic effect by reducing serum glucose and increasing serum insulin level in comparison to positive control (diabetic) group. Use of high protein diet also normalized serum amylin, leptin, GCK, T3, T4 and TSH. In sum, these results indicated the anti-hyperglycemic potential of high protein diet in alloxan-induced diabetic rat model. ©2019 PVJ. All rights reserved Key words: Amylin, leptin High protein diet Hyperglycemia Thyroid hormone To Cite This Article: Muzaffar H, Faisal MN, Khan JA and Aslam B, 2019. High protein diet improves biochemical and metabolic hormonal profile in Alloxan-induced diabetic rats. Pak Vet J, 39(2): 231-235. http://dx.doi.org/10.29261/pakvetj/2019.016 Masih, Institute of Pharmacy, Physiology and Pharmacology, University of Agriculture Faisalabad, Pakistan for helping in animals handling and management. Authors contribution:The work is a product of the intellectual environment of the whole team; and all the members have contributed in various degrees in designing the study, developing the methodology, performing the analysis and writing the manuscript.

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Section: Discussionsupporting

confidence: 45%

High Protein Diet Improves Biochemical and Metabolic Hormonal Profile in Alloxan-Induced Diabetic Rats

Muzaffar¹

2019

PVJ

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“…Ryan et al [20] found that leptin could lead to vascular dysfunction by directly acting on LEPR. In addition, some studies also confirmed that the serum leptin level increased in patients with diabetes, indicating its involvement in the occurrence and development of diabetic vascular complications [21] . Wu et al [6] showed that hydrogen sulfide could inhibit the HG-induced injury in HUVECs through inhibiting leptin/LEPR.…”

Section: Discussionmentioning

confidence: 88%

N-acetylcysteine resists high-glucose-induced injury of human umbilical vein endothelial cells by inhibiting the leptin/leptin receptor

Wang¹,

Lian

Liao

et al. 2020

Preprint

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Baclground The present study aimed to investigate whether N- acetylcysteine (NAC) protects human umbilical vein endothelial cells (HUVECs) against high glucose (HG)-induced injury by inhibiting leptin/leptin receptor (LEPR).Methods HUVECs were treated with 40 mmol/L glucose for 24 h to establish a model of HG-induced endothelial cell injury; The cell viability was examined by cell counter kit-8(CCK-8) assay; The expression levels of leptin, LEPR, cleaved caspase-3 and endothelial nitric oxide synthase (eNOS) were detected by western blot. The intracellular levels of reactive oxygen species (ROS) were tested by DCFH-DA staining followed by photofluorography. Tumor necrosis factor-α (TNF-α)、nuclear factor-kappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) were detected by enzyme-linked immunosorbent assay (ELISA). The number of apoptotic cells was observed by photofluorograph with Hoechst 33258 nuclear staining. Mitochondrial membrane potential (MMP) was obtained using JC-1. Results The expression of leptin and LEPR began to significantly increase after exposure to 40 mmol/L HG for 24 h. Pretreatment of HUVECs with 7 mmol/L NAC or 50 ng/mL leptin antagonists (LA) for 30min inhibited the increased expression of leptin and LEPR induced by HG in HUVECs. Furthermore, pretreatment with 7 mmol/L NAC or 50 ng/mL LA for 30 min also inhibited HG-induced injury, by increasing the cell viability and eNOS expression, and decreasing the inflammatory response and cleaved caspase-3 expression, the apoptotic cells and generation of intracellular ROS and a loss of MMP. Conclusions NAC protects the HUVECs against HG-induced injury by inhibiting leptin/LEPR.

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“…Ryan et al [22] found that leptin could lead to vascular dysfunction by directly acting on LEPR. In addition, some studies also confirmed that the serum leptin level increased in patients with diabetes, indicating its involvement in the occurrence and development of diabetic vascular complications [23] . Wu et al [6] showed that hydrogen sulfide could inhibit the HG-induced injury in HUVECs through inhibiting leptin/LEPR.…”

Section: Discussionmentioning

confidence: 88%

N-acetylcysteine resists high-glucose-induced injury of human umbilical vein endothelial cells by inhibiting the leptin/leptin receptor

Wang¹,

Lian

Liao

et al. 2020

Preprint

View full text Add to dashboard Cite

Background The present study aimed to investigate whether N-acetylcysteine (NAC) protects human umbilical vein endothelial cells (HUVECs) against high glucose (HG)-induced injury by inhibiting leptin/leptin receptor (LEPR).Methods HUVECs were treated with 40 mmol/L glucose for 24 h to establish a model of HG-induced endothelial cell injury; The cell viability was examined by cell counter kit-8 (CCK-8) assay; The expression levels of leptin, LEPR, cleaved caspase-3 and endothelial nitric oxide synthase (eNOS) were detected by western blot. The intracellular levels of reactive oxygen species (ROS) were tested by DCFH-DA staining followed by photofluorography. Tumor necrosis factor-α (TNF-α) nuclear factorkappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) were detected by enzyme-linked immunosorbent assay (ELISA). The number of apoptotic cells was observed by photofluorograph with Hoechst 33258 nuclear staining. Mitochondrial membrane potential (MMP) was obtained using JC-1. ResultsThe expression of leptin and LEPR began to significantly increase after exposure to 40 mmol/L HG for 24 h. Pretreatment of HUVECs with 7 mmol/L NAC or 50 ng/mL leptin antagonists (LA) for 30min inhibited the increased expression of leptin and LEPR induced by HG in HUVECs.Furthermore, pretreatment with 7 mmol/L NAC or 50 ng/mL LA for 30 min also inhibited HG-induced injury, by increasing the cell viability and eNOS expression, and decreasing the inflammatory response and cleaved caspase-3 expression, the apoptotic cells and generation of intracellular ROS and a loss of MMP.Conclusions NAC protects the HUVECs against HG-induced injury by inhibiting leptin/LEPR.

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Leptin, cardiovascular diseases and type 2 diabetes mellitus

Cited by 236 publications

References 212 publications

High Protein Diet Improves Biochemical and Metabolic Hormonal Profile in Alloxan-Induced Diabetic Rats

High Protein Diet Improves Biochemical and Metabolic Hormonal Profile in Alloxan-Induced Diabetic Rats

N-acetylcysteine resists high-glucose-induced injury of human umbilical vein endothelial cells by inhibiting the leptin/leptin receptor

N-acetylcysteine resists high-glucose-induced injury of human umbilical vein endothelial cells by inhibiting the leptin/leptin receptor

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