MedNexus
Volume 06 · Issue 07 · 2014
MedNexus
- Sections
- Editorial
- Special Article
- Guideline and consensus
- Original Article
- 会议传真
- Review Article
- Case Report
- New Perspective
- 他山之石
- unknow column
At present, there are nearly 100 million diabetic patients in China, which is the country with the largest number of diabetic patients in the world. About 15% of diabetic patients will develop foot ulcers in their lifetime, and the risk of lower limb amputation is 40 times higher than that of non-diabetic patients. About 85% of these amputations are caused by foot ulcers[
The research on diabetic foot disease in China started in the late 1970s and early 1980s. In 1996, the Diabetes Branch of Chinese Medical Association established the first podiatry group. The first group made great achievements in promoting the knowledge of prevention and treatment of diabetic foot disease, standardizing the classification and diagnosis criteria of diabetic foot disease, and strengthening the academic exchange between domestic colleagues[
Diabetic foot disease is one of the major health problems of our time. Foreign studies have pointed out that the annual incidence rate of diabetic foot is 2% ~3%, and about 15% ~20% of diabetic foot patients may have foot ulcers, and about 40% ~80% of them are infected with ulcers[
For thousands of years, medicine has been exploring to find a cure for human diseases, and the pace of exploration has never stopped. Improving people's quality of life and prolonging life has always been the sacred mission of medical practitioners.
To compare and analyze clinical data, ulcer characteristics, prognosis and hospitalization expenses in the patients with diabetic foot ulcer in 2004 and 2012 in China.
Diabetic foot disease data from 14 great three A hospitals from 10 provinces or cities in 2004 and 15 great three A hospitals from 11 provinces or cities in 2012 in China were collected and analyzed, including the medical history, physical and biochemical examinations, demographic characteristics, prognosis and hospitalization expenses. The classification, stage and risk factors of diabetic foot ulcer were also compared between two groups. The t, χ 2 and u tests were used for comparing between two groups of data. Hospitalization expenses of diabetic foot disease was corrected with consumer price index.
386 cases in 2004 and 682 cases in 2012 were recruited. No significant differences in age, educational level, duration of diabetes, waist hip ratio, glycosylated hemoglobin A1c, triglyceride, high density lipoprotein cholesterol, uric acid, prevalence of dyslipidemia, cerebrovascular, peripheral artery disease, diabetic peripheral neuropathy, ischemic foot ulcer, and hospitalization expenses between two groups (all P>0.05). Compared with the patients in 2004, duration of diabetic foot (1(1-6) vs 6(1-16) m,u=-7.955, P<0.05) was shorter, more men(65.2% vs 58.5%, χ2=4.738, P<0.05), more patients with smoking(45.8% vs 39.0%, χ2=4.602, P<0.05) and/or drinking(41.1% vs 19.1%, χ2=51.179, P<0.05), lower fasting and postprandial blood glucose, total cholesterol and low density lipoprotein cholesterol in 2012(t=-2.987, -2.855, -4.910, -3.748, all P<0.05). The higher prevalence of hypertension, coronary heart disease, diabetic kidney disease, diabetic retinopathy(χ2 =47.572, 13.297, 9.638, 4.329; all P<0.05), and more patients with infectious foot ulcer, more patients with severe foot disease whose foot ulcer classified as Wagner 3 and above or Texas D (χ2 = 6.787, 40.880, 11.028, all P<0.05). There were significantly lower major amputation rate, higher ulcer healing rate(χ2 = 8.838, 8.908, 107.773, all P<0.05), shorter hospital stay (18(12-32) vs 21(15-32)d,u=-3.349, P<0.05).
The patients with diabetic foot disease in 2004 and 2012 were older, with more men, low educational level, long duration of diabetes, poor control of hyperglycemia, high hospitalization expenses and with more cardiovascular risk factors and diabetic complications. Compared with the patients in 2004, patients with diabetic foot disease in 2012 had more concomitant diseases and complications, with more severe foot ulcers and infections, higher total amputation rate, but lower major amputation rate, higher ulcer healing rate, and shorter hospital stay.
To assess the concordance between culture results from wound superficial swab and deep tissue biopsy samples in patients with diabetic foot infection (DFI).
Forty-two patients with DFI were enrolled in this study at Diabetic foot care center, Department of Endocrinology and Metabolism of West China Hospital, Sichuan University from November 2013 to March 2014. Superficial swab and deep tissue biopsy specimens were taken from each wound at the end of debridement for culture. Pathogens were isolated and identified at species level by standard methods. The agreement between culture results from wound swabs and tissue samples from the same patient was evaluated by statistical analysis method of diagnostic trial.
(1)A total of 70 pairs of samples (swab and tissue samples) were available from 42 eligible patients, 52 strains of pathogens were isolated from diabetic foot ulcers in 24/42(57.1%) patients. (2)The positive ratio of pathogen culture from the superficial swab was similar with deep tissue biopsy specimens(65.7% vs 70.0%), Gram-negative aerobes were most frequently isolated (54.3% vs 53.1%), followed by gram-positive aerobes (34.8% vs 34.5%). There are no differences between the methods (χ2=0.444, P>0.05). (3)Overall, 61 (87.14%) of the superficial swab and deep tissue biopsy pairs had identical culture results, but in 18 (29.5%) cases the cultures were sterile; thus, only 43(82.7%) of the 52 culture-positive pairs had identical results. When compared to deep tissue biopsy specimens culture results, the superficial swab cultures had a overall accuracy of 87.14%. Sensitivity, specificity, positive likelihood ratios (PLR), negative likelihood ratios (NPR), Contingency Coefficient and Kappa value of swab cultures for the identifying pathogens were 93.48%, 75.00%, 3.739 1, 0.087 0, 0.579 and 0.706, respectively.
The findings suggest that superficial swab culture are valuable and accurate in identifying the organisms causing diabetic foot infection, given that they are more widely simple and applicable than tissue cultures.
To investigate the structure changes of foot skin microcirculation features of diabetic foot ulcer through comparing the foot skin microcirculation structure between diabetic and non diabetic foot.
29 diabetes with foot ulcer and 19 non-diabetes with orthopedics foot malformation or trauma surgery in-patients were recruited in Sun Yat-sen Memorial Hospital from June 2011 to April 2012. Foot skin was collected to make paraffin section. The von Willebrand factor (vWF) and vascular endothelial growth factor (VEGF) and its antibody in vascular endothelial cells were showed by immunohistochemistry and the photographs were analysis by Image Pro 6.0 to compare the data of foot skin papillary layer of dermis between two groups. The t test compares the differences between two groups. Association between variables is examined by multiple logistic regression analysis.
Compared with non-diabetic patients, the papillary dermal area ((1.6±0.5)×105 vs (1.1±0.4)×105 μm 2, t=3.5, P<0.05) of diabetic patients was increased, but the papillary dermal density (63±18 vs 90±30,t=4.05, P<0.05) was decreased significantly; In diabetes, the microvascular density(109±34 vs 161±40,t=4.81, P<0.05)was lower, but the out diameter of microvascular((23.9±2.8)vs(21.9±3.2) μm,t=2.28, P<0.05) in dermal papilla was bigger. The endothelial cells number(8.2±1.5 vs 10.3±2.1,t=4.06, P<0.05)and the vascular endothelial cells number per unit area(320±150 vs 563±212,t=4.65, P<0.05)were reduced, on the contrary, the vascular endothelial cells thickness((4.0±0.4)vs(3.2±0.3)μm,t=6.47, P<0.05)was increased. At the same time, the expression of VEGF(0.34±0.04 vs 0.41±0.05,t=4.87, P<0.05)was decreased significantly.
The incidence and development of diabetes foot is involved with the change of foot skin microcirculation structure in papillary layer of dermis.
To evaluate the efficacy and safety of biphasic insulin aspart 30 (BIAsp30), and quality of life in Chinese elderly patients (> 65 years-old) with type 2 diabetes in regular clinical practice, and to compare with the data from Chinese young patients (≤65 years-old).
A1chieve study is a 24 weeks, prospective, multi-center, open-label, non-interventional research. Patients were grouped by age, and further grouped into insulin-naive and insulin-experienced, respectively.
A total of 1 969 elderly patients and 6 508 young, who were treated with BIAsp30 during the A1chieve research in China, were analyzed. No serious adverse drug reaction was reported. The rate of total, nocturnal, and major hypoglycemic events were 2.84/0.91/0.34 event/patient-year, reported by elderly patients with diabetes at baseline, and were decreased to 2.00/0.41 (P=0.0371)/0 event/patient-year, respectively, after 24 weeks treatment with BIAsp30. The corresponding rates reported by young patients were reduced from 2.19/0.48/0.10 event/patient-year at baseline to 1.39/0.23 (P<0.001)/0 event/patient-year at 24 weeks, respectively. HbA1c decreased from (9.3±2.3)% and (9.6±2.3)% at baseline to (7.0±1.0)% and (7.0±1.0)% at end of study in elderly and young patients, respectively (elderlyt=-33.47, P<0.001; youngt=-67.94, P<0.001). The proportion of elderly and young patients who achieved HbA1c < 7% increased from 13.8% (223/1 620) and 9.5% (514/5 390) at baseline to 57.7% (682/1 182) and 55.0% (2 124/3 863) at end of the study. Fasting plasma glucose decreased from (9.8±3.5) and (10.4±3.6) mmol/L at baseline to (6.8±1.2) and (6.7±1.3) mmol/L at end of study (elderlyt=-32.86, P<0.001; youngt=-70.02, P<0.001); postprandial plasma glucose (after breakfast) reduced from (13.9±4.8) and (14.4±4.9) mmol/L at baseline to (8.9±1.7) and (8.8±1.8) mmol/L at end of study (elderlyt=-34.14, P<0.001; youngt=-67.70, P<0.001), in elderly and young patients, respectively. The quality of life were significantly ameliorated in both elderly and young patients.
BIAsp30 improved glycemic control effectively, without increasing the risk of hypoglycemia, and particularly reduced the risk of nocturnal and major hypoglycemia. The application of BIAsp30 is similarly effective and safe in both Chinese elderly and young patients with type 2 diabetes.
To observe the different effects between patients with or without family history of diabetes with insulin pump therapy, and explore the genetic background of early insulin secretion function.
A total of 158 newly diagnosed type 2 diabetic patients from July 1st 2008 to December 1st 2011 were recruited. According to the presence or absence of family history of diabetes, they were divided into 2 group: one was with a family history group(FH+ DM group) and another was without a family history group(FH-DM group). All the patients were treated with continuous subcutaneous insulin infusion (CSII) for 10 days. L-arginine (L-ARG) stimulating test was used to test the insulin values before and after intensive insulin therapy. t test was used between 2 groups. Analysis of multiple variables using multiple regression analysis.
(1)The peak of insulin secretion: before intensive insulin therapy, the multiples of the peak of the FH+ DM group and FH-DM group were 5.0±2.5, 5.2±2.5, respectively. After the therapy, they were increased by 14.3% and 16.1%. (2) The first phase of insulin secretion: before the therapy, the level of 2 min insulin incretion and the first phase of insulin secretion in FH+ DM group was lower than FH-DM.After the therapy, the level of first phase insulin secretion were 20.41 mU/L and 22.39 mU/L of the two groups.They were lowered by 18.4% and 20%, and FH-DM had a more obvious reduction.(3) HOMA-IR: HOMA-IR in the two groups were both lower than before.They were 4.26 vs 2.02, and 5.14 vs 2.15(P<0.05).
Insulin pump therapy has positive effects on the first phase function of islet β-cell.And the result is more obvious in the group without family history.
To evaluate the effects of combined low glycemic index(LGI) and low glycemic load(LGL) diet intervention on glucose and lipid metabolism in community patients with type 2 diabetes mellitus(T2DM).
A total of 105 patients with T2DM were enrolled from 3 different communities in Changsha city in this study, 35 T2DM patients in each community with met inclusion criteria. The three communities were randomly divided into the whole day diet intervention group (group A), breakfast intervention group (B group) and control group (group C) by draw lots. The patients with T2DM in group A and group B received 3 months combined LGI and LGL diet intervention at the basis of keeping the original regimen. All the subjects in the study were tested fasting blood glucose(FBG), 2-hour postprandial blood glucose (2 hPG), glycosylated hemoglobin (HbA1c), triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C) and low density lipoprotein-cholesterol (LDL-C) before and after dietary intervention. The quantitative data obeying normal distribution were compared with one-way analysis of variance.
Multiple independent sample Kruskal-Wallis H test showed that the HbA1c of three groups improved after the intervention(all P<0.05), and it was better in group A than that in group B and C(H=26.749, P<0.0167). The HDL-C in the three groups decreased significantly after the intervention(allP<0.05), and it decreased further in group A than that in group B and C (H=12.671, P< 0.0167). The metabolism of TG in patients with T2DM of the three groups improved significantly when compared with those before intervention(allP<0.01), and it was better in group A and B than that in group C (H=14.921, P<0.05).
Combined LGI and LGL diet intervention can effectively improve HbA1c, HDL-C and TG of the patients with T2DM, especially the whole day diet intervention is more effective than only breakfast diet intervention.
To investigate the presence of lectin-like oxidized low-density lipoprotein(ox-LDL) receptor-1 (LOX-1) in cultured hepatic sinusoidal endothelial cells (HSECs), and meanwhile discuss the regulation of its mechanisms under ox-LDL injury conditions.
The mRNA and protein expression of LOX-1 was testified by real-time quantitative polymerase chain reaction(RT-PCR) and Western blotting methods. Meanwhile HSECs were stimulated with different concentration of ox-LDL (0, 20, 40, 60, 80 and 100 mg/L) for 24 h, and HSECs were stimulated with 80 mg/L for different times (0, 12, 24 and 48 h). Then expression of LOX-1 mRNA was measured by RT-PCR, and the protein expression of LOX-1 was testified by using Western blotting. Data were analyzed with one-way ANOVA and t test.
LOX-1 exists in HSECs. After intervened with 20-80 mg/L ox-LDL for 24 h, LOX-1 mRNA and protein levels increased significantly in a dose-dependent manner(F=38.7, 3.48, both P<0.05). However, when concentration of ox-LDL reached 100 mg/L, the LOX-1 mRNA and protein expression decreased significantly compared with those intervened with 80 mg/L ox-LDL (t=23.75, 18.26, both P<0.05). Meanwhile, after intervened with 80 mg/L ox-LDL at different time (0-24 h), the expression of LOX-1 mRNA and protein significantly increased in a time-manner(F=2.36, 0.328, both P<0.05). And compared with those in cells intervened for 24 h, the mRNA and protein expression of LOX-1 decreased significantly when intervened for 48 h(t=69.21, 36.27, both P<0.05). However, compared with the cells incubated with 80 mg/L ox-LDL, the mRNA and protein expression of LOX-1 significantly decreased in HSECs treated with polyinosinic cytidylic acid(t=54.93, 28.19, both P<0.05).
LOX-1 exists in HSECs and ox-LDL could regulate it in a certain reach of concentration and time. However, polyinosinic cytidylic acid can partly restrained ox-LDL-induced LOX-1 expression.
To cultivate mice podocyte with high glucose and lipoic acid, to observe the apoptosis rate and the change of endoplasmic reticulum stress (ERS) marker : GRP78 and Caspase-12. To investigate the relationship between endoplasmic reticulum stress and podocyte apoptosis.
Already differentiated mice podocyte were divided into 4 subgroups: normal glucose concentration group, (5.6 mmol/L), mannitol hypertonic control group(25 mmol/L), high glucose group(25 mmol/L), high glucose + lipoic acid group (25 mmol/L+ 500 μmol/L). Index and detection method: after 48 h, to detect cell apoptosis rate by flow cytometer, to detect the expression of GRP78 and Caspase-12 mRNA with reverse transcription-polymerase chain reaction (RT-PCR) technology, to detect the GRP78 and Caspase-12 protein expression with Western blotting technology. The apoptosis rate and expression of GRP78 and Caspase-12 mRNA and protein between the groups were compared by LSD- t test.
About cell apoptosis rate: (1)The apoptosis rate between normal glucose concentration group and hypertonic group were not statistically significant((3.4±0.6)% vs (3.7±0.9)%, t=0.52, P>0.05); The apoptosis rate of high glucose group was significantly higher than normal glucose concentration group((14.0±1.1)% vs (3.4±0.6)%,t=9.12, P<0.05); The apoptosis rate of lipoic acid + high glucose group was significantly decreased than high glucose group((14.0±1.1)% vs (7.8±0.6)%,t=7.73, P<0.05). (2)The expression of GRP78 and Caspase-12 mRNA in high glucose group increased significantly than normal glucose concentration group (2.62±0.57 vs 0.85±0.24, 10.04±2.28 vs 1.28±0.97;t=6.75, 25.84, all P<0.05); The expression of GRP78 and Caspase-12 mRNA in lipoic acid + high glucose group, decreased significantly than high glucose group(0.82±0.22 vs 2.62±0.57, 4.98±0.55 vs 10.04±2.28,t=3.83, 11.83, all P<0.05). (3)The expression of GRP78 and Caspase-12 protein in high glucose group increased significantly than normal glucose concentration group(2.48±0.19 vs 0.37±0.04, 2.07±0.18 vs 0.47±0.08,t=17.55, 12.34, all P<0.05); The expression of GRP78 and Caspase-12 protein in lipoic acid + high glucose group decreased significantly than high glucose group(0.61±0.15 vs 2.48±0.19, 0.89±0.18 vs 2.07±0.18,t=4.42, 3.25, all P<0.05).
(1)High glucose can improve apoptosis of podocyte by the endoplasmic reticulum stress reaction. (2) The lipoic acid can reduce the endoplasmic reticulum stress reaction to protect the podocyte.
To investigate the impacts of C1q/tumor necrosis factor (TNF) related protein-3 (CTRP3) on the expression of adiponectin(APN), leptin(LPT), visfatin(VFT) and apelin(APL) in 3T3-L1 adipocytes. The effect of insulin resistance on the impacts was also investigated.
The insulin resistant 3T3-L1 adipocytes were induced by palmic acid. There were six groups: normal control group, insulin resistance group, CTRP3(10, 50, 250 μg/L) treated normal group and CTRP3 (250 μg/L) treated insulin resistance group. The secretion and gene expression of the adipokines were detected by enzyme-linked immunosorbent assay(ELISA) and real-time polymerase chain reaction(RT-PCR) respectively. One-way ANOVA was used for statistical analysis of the differences among groups and SNK- q test was used for the further comparison between two groups.
Compared with normal control group, the secretion of APN, LPT, VFT and APL in 250 μg/ml CTRP3 intervention group was increased by 63.3%, 42.9%, 57.1% and 56.0%( q=8.605, 8.526, 8.284, 8.573, all P<0.05) respectively. The secretion of such adipokines had increased trend in 10 and 50 μg/L CTRP3 intervention groups, while only the increase of APL in 50 μg/L CTRP3 intervention group was significant ((6.2±1.1) vs (5.0±0.9) μg/L,q=4.593, P<0.05). The gene expression had the same trend after treatment, and the mRNA relative expression of APN, LPT, VFT and APL at the intervention concentration of 50 μg/L was increased by 22.0%, 13.0%, 20.0% and 33.0% respectively in comparison with that in normal control group(q=6.150, 3.987, 5.653, 9.031, all P<0.05). Compared with the CTRP3 treated normal group, the protein release of APN, LPT, VFT and APL in CTRP3 treated insulin resistant group were decreased by 28.6%, 21.0%, 24.5% and 17.9% respectively (q=6.341, 5.969, 5.592, 4.287, all P<0.05), and gene expression were decreased by 21.6%, 17.2%, 15.6% and 18.9% respectively (q=9.225, 7.668, 7.066, 8.210, all P<0.05).
CTRP3 may dose-dependently increase the secretion and gene expression of APN, LPT, VFT and APL in 3T3-L1 adipocytes. Insulin resistance may inhibit this effect.
To explore the effects of glucagon-like peptide-1 receptor analog liraglutide(LR) on the expression of local renin-angiotensin system (RAS) and transforming growth factor (TGF)-β1 in renal tissue of diabetic rats.
Twenty Wistar rats diabetes models were divided into, diabetic group (DM), and LR-treated group(LR) according to the table of random number after induced by feeding with high-sugary and high-fat diet and injecting of a low dose of streptozotocin into the caudal vein for 8 weeks. And ten healthy Wistar rats were set as normal control(NC). After the establishment of diabetes model, liraglutide (400 μg·kg -1·d-1) was administered by subcutaneous injection for 12 weeks in LR group. And the rats in NC and DM group were injected with saline in the same way. At the end of the trial, the mRNA expression levels of angiotensin Ⅱ(AngⅡ) type 1 receptor (AT1R) and TGF-β1 were detected by real-time quantitative polymerase chain reaction(RT-q PCR), the protein expression levels of AT1R and TGF-β1 were detected by Western blotting(WB) and the protein expression of AngⅡ was detected by enzyme-linked immunosorbent assay(ELISA). Masson staining was used to observe the collagen deposition of renal tissue in rats of different groups. Single factor analysis of variance(ANOVA) was applied in data comparison among the groups, and LSD test were used to analyze the difference between two groups.
Masson staining showed that DM group had more collagen than NC group in renal tissue, but it was alleviated in LR group. Compared with that in NC group, expressions of AngⅡin renal tissue of DM group was elevated significantly(t=3.444, P<0.05), and it was down-regulated significantly in LR group thant that in DM group(t=2.614, P<0.05). The mRNA and protein expression of AT1R and TGF-β1 in renal tissue in DM group were significantly higher than those in NC group(t=4.084, 3.714, 9.381, 6.408, all P<0.05), and all were down-regulated significantly in LR group when compared with those in DM group(t=3.487, 2.907, 5.033, 2.295, all P<0.05).
Liraglutide plays a role of organ-protecting by inhibiting the expression of TGF-β1 in renal tissue of diabetic rats, and this may be related with the down-regulating of local RAS.
On April 9, 2014, the "Yikai Cup" Diabetes Physician Salon of Chinese Diabetes Journal was successfully held in Nanjing. This salon was hosted by Professor Sun Zilin, Department of Endocrinology, Zhongda Hospital affiliated to Southeast University, and Professor Liu Chao, Department of Endocrinology, Jiangsu Hospital of Integrated Traditional Chinese and Western Medicine. More than 70 endocrinologists and general practitioners from hospitals at all levels in Jiangsu Province participated in this salon activity.
Fibroblast growth factor 21 (FGF21) is a protein containing 181 amino acids with a molecular weight of about 20,000. It originates from a mature 209 amino acid protein encoded by the FGF gene localized on chromosome 19[
The pathogenesis of type 2 diabetes mellitus (T2DM) is unknown, but insulin resistance and/or insulin secretion defects are prevalent, and the number of islet β cells is progressively lost as the disease progresses. The decrease in the number of β cells is not only due to the decrease of proliferation, but more importantly, the increase of apoptosis. Therefore, protecting beta cells has become a research hotspot. At present, oral hypoglycemic drugs commonly used in clinical practice mainly control blood sugar by promoting insulin secretion or increasing insulin sensitivity, and cannot solve the problem of progressive reduction of β cells. However, recent studies have found that newly marketed new hypoglycemic drugs dipeptidyl peptidase 4 (DPP-IV) inhibitors or glucagon-like peptide 1 (GLP-1) analogs can not only effectively reduce blood sugar and glycosylated hemoglobin (HbA1c), but also protect pancreatic islet β cells through the GLP-1 receptor signal transduction pathway, but its specific mechanism needs further research. The molecular mechanisms of GLP-1 receptor signal transduction on the secretory function, proliferation and apoptosis of pancreatic islet β cells were reviewed.
Emphysematous pyelonephritis (EPN) is an acute infection of renal parenchyma and surrounding tissues caused by Aerobacter aerogenes, which is extremely rare in clinical practice. This disease mostly occurs in diabetic patients, and the lesions are mostly located in the left kidney. We treated an elderly patient with diabetes complicated with painless right emphysematous pyelonephritis, and the literature review report is as follows.
At present, the prevalence of adult diabetes in China is estimated at 11.6%, that is, there are about 113.9 million adults with diabetes in China[
Regulating apoptosis is an emerging weight loss strategy because it can reduce body fat by eliminating adipocytes. The effect of vitamin D on apoptosis is mediated by multiple signaling pathways, which ultimately act on cellular Ca2+。 Researchers earlier found that 1,25-dihydroxyvitamin D3Induced Ca2+Signaling and Ca in mature adipocytes2+Related to the activation of apoptosis-dependent proteases. In this study, researchers used a diet-induced obesity (DIO) mouse model to evaluate the role of vitamin D and calcium in obesity.
In order to evaluate the activity of endothelial lipase and hepatic lipase in post-heparin plasma of patients with metabolic syndrome and obesity, and their relationship with atherogenic lipoprotein and anti-atherogenic lipoprotein, and to evaluate the activity of lipoprotein esterase and hepatic lipase under the action of triglyceride hydrolysate to complete the analysis of SN1 lipase in the same patient, the researchers evaluated the activity of endothelial lipase, hepatic lipase and lipoprotein esterase in 59 patients with metabolic syndrome and 36 controls.
Microfiber-associated glycoprotein 1 (MAGP1) is one of the components of extracellular matrix microfibers. Here, we confirmed that MAGP1 expression undergoes important changes in obese populations, and in mice the MAGP1 gene (Mfap2-/-) inactivation leads to fat cell hypertrophy and a tendency to metabolic dysfunction. Proven Mfap2-/-Impaired thermoregulation in mice preceded fat changes, suggested to induce MAGP1 to increase the predisposition to obesity and diabetes. Mfap2-/-Mice adapt to the adverse environment of cold challenge, and the expression of uncoupling protein 1 (UCP-1) attenuates brown adipose tissue and reduces brownness in subcutaneous white adipose tissue. The activity of transforming growth factor beta (TGF-β) was elevated in the adipose tissue of Mfap2, which-/-Treatment of mice with TGF-β neutralizes antibodies, increases body temperature, and prevents increased obesity phenotypes. Taken together, these results reveal that MAGP1 can prevent the effects of metabolic stress through the regulation of TGF-β, and its lack is prone to induce metabolic dysfunction.
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