ABSTRACT
BACKGROUND: Madelung disease (MD) is a rare disorder of fat metabolism, resulting in diffuse, symmetrical and painless deposition of adipose tissue in subcutaneous superficial fascial space and/or deep fascia space of the head, neck and shoulders, etc. CASE SUMMARY: We report a case of MD accompanied by type 2 diabetes in a 61-year-old Chinese male. The patient presented with progressive fat deposition over the mandible, neck, abdomen and elbows. He had a history of smoking and alcohol abuse. Excessive fat deposition was seen in the mandible, elbows and the abdominal area of the patient by ultrasonic examination. Computed tomography showed diffuse and marked soft masses (fat density) in the subcutaneous superficial fascia space of the neck. The patient was diagnosed with MD. He was advised to abstain from alcohol and was followed up regularly. CONCLUSION: This report discusses the pathogenesis, diagnosis and treatment of MD, and raises the clinician's awareness of this disease.
ABSTRACT
OBJECTIVE: Aquaglyceroporin 7 (AQP7) is required for efflux of glycerol from adipocytes. In this study, we aimed to analyze expression profiles of AQP7 in the different differentiation phases of adipocytes and to investigate the role of AQP7 in the insulin resistance of adipocytes. METHODS: 3T3-L1 pre-adipocyte cells were induced to be fully differentiated adipocytes and then insulin resistance was induced by Dexamethasone (DXM) or TNF-α. Adenovirus vector with over-expression AQP7 (Ad-AQP7) was constructed and transfected into adipocytes. The expression level of AQP7 and phosphorylated PKB (p-PKB) were measured. The glycerol released from adipocytes and glucose consuming rate were tested too. RESULTS: AQP7 expression was gradually up-regulated along with the differentiation processing of 3T3-L1 preadipocytes, which was consistent with the expression level of p-PKB. Dexamethasone down-regulated the expression of AQP7, p-PKB and the glycerol content in adipocytes. Over-expression of AQP7 by transfecting Ad-AQP7 to insulin resistant adipocytes restored the phosphorylation of PKB and attenuated the glycerol secretion and glucose consuming rate of adipocytes. CONCLUSIONS: AQP7 is down-regulated in adipocytes with insulin resistance. The over-expression of AQP7 contributes to improve insulin resistance in adipocytes, which is potentially correlated with the increased phosphorylation of PKB.
Subject(s)
Adipocytes/cytology , Aquaporins/genetics , Insulin Resistance/genetics , 3-Phosphoinositide-Dependent Protein Kinases , 3T3-L1 Cells , Adipocytes/metabolism , Animals , Aquaporins/metabolism , Cell Differentiation , Dexamethasone/pharmacology , Down-Regulation , Mice , Phosphorylation , Protein Serine-Threonine Kinases/genetics , Protein Serine-Threonine Kinases/metabolism , RNA, Messenger/metabolism , Tumor Necrosis Factor-alpha/metabolismABSTRACT
AIM: To study the effect of angiotensin-(1-7) on the kidney of diabetic rats by observing the mRNA expression of PDGF and TGF-beta1. METHODS: SD rats were divided into three groups: Group C (uni-nephrectomy control group), Group D (diabetic model control group), Group T (Ang-(1-7) treated group). We evaluated blood glucose,urea nitrogen, creatinine and urine albumin excretion respectively, studied the renal morphology by light microscope, and detected the gene expression of PDGF, TGF-beta1 in renal tissue by RT-PCR technique. RESULTS: There was significant difference between the group D and T about the RW/BW, renal morphology, the total urine protein and the mRNA expression of PDGF and TGF-beta1. CONCLUSION: Ang-(1-7) can relieve the renal process of diabetic rats.
Subject(s)
Angiotensin I/pharmacology , Diabetes Mellitus, Experimental/metabolism , Diabetic Nephropathies/metabolism , Peptide Fragments/pharmacology , Platelet-Derived Growth Factor/metabolism , Transforming Growth Factor beta1/metabolism , Animals , Kidney/metabolism , Kidney/pathology , Male , Platelet-Derived Growth Factor/genetics , RNA, Messenger/genetics , RNA, Messenger/metabolism , Rats , Rats, Sprague-Dawley , Transforming Growth Factor beta1/geneticsABSTRACT
PURPOSE: Angiotensin II receptor Type 1 antagonists postpone the development of nephropathy in type 2 diabetes mellitus (DM). We hypothesize that Losartan may ameliorate renal function in diabetic patients through the regulation on the generation of transforming growth factor (TGF)-beta and fibrinolytic regulators. METHODS: Twenty-two type 2 DM patients with microalbuminuria were treated with 50-100 mg/day of Losartan for 6 months. Urinary secretion of TGF-, plasminogen activator inhibitor-1 (PAI-1), tissue and urokinase plasminogen activators (tPA and uPA) fibronectin, collagen IV and plasma levels of TGF-beta, PAI-1, tPA and uPA of the patients before and after the treatment were analyzed using enzyme-linked immunoabosorbance assay. RESULTS: Losartan effectively reduced arterial blood pressure and urinary albumin excretion. The levels of TGF-beta in urine, but not in plasma, were reduced after 2, 4 and 6 months of the treatment (-32% to -48%, P < 0.05 or 0.01). Urinary or plasma levels of PAI-1, tPA or uPA, and urinary secretion of fibronectin or collagen IV were not significantly altered by Losartan treatment. Urinary levels of collagen IV positively correlated with uPA, and that of fibronectin negatively correlated with PAI-1 in the patients (P < 0.01). Urinary TGF-beta negatively correlated uPA in urine of the patients (P < 0.01). CONCLUSION: Losartan reduced urinary excretion of TGF-beta and albumin in type 2 DM patients with microalbuminuria. Fibrinolytic regulators and TGF-beta are implicated in the regulation of ECM turnover in kidneys of the patients with diabetic nephropathy.
