scholarly journals Antidiabetic and Antiobesity Effects of Artemether in db/db Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Yu Guo ◽  
Wei Fu ◽  
Yakai Xin ◽  
Jinlei Bai ◽  
Huifang Peng ◽  
...  

This study is designed to investigate the effect of artemether on type 2 diabetic db/db mice. The experiments consisted of three groups: normal control (NC, db/+, 1% methylcellulose, intragastric administration), diabetic control (DM, db/db, 1% methylcellulose, intragastric administration), and artemether treated (artemether, db/db, 200 mg/kg of artemether, intragastric administration). The treatment lasted for two weeks. The food intake, body weight, and fasting blood glucose of mice were measured every three days. At the start and end of the experiment, the intraperitoneal glucose tolerance test (IPGTT) and insulin tolerance test (IPITT) were performed. We determined the serum insulin and glucagon levels by ELISA kits and calculated insulin resistance index (HOME-IR). HE staining was used to observe the morphologies of pancreas and liver in mice. The damage of pancreatic beta cells was evaluated by TUNEL staining and immunofluorescence. We found the following: (1) compared with the DM group, the food intake and weight increase rate of artemether group significantly reduced (P<0.05); (2) compared with pretreatment, artemether significantly reduced the fasting blood glucose levels, and the areas under the curves (AUCs) of IPGTT were decreased significantly, increasing the tolerance to glucose of db/db mice. (P<0.05); (3) artemether improved hyperinsulinemia and decreased the AUCs of IPITT and HOME-IR, increasing the insulin sensitivity of db/db mice. (4) Artemether significantly ameliorated islet vacuolar degeneration and hepatic steatosis in db/db mice. (5) Artemether reduced the apoptosis of pancreatic beta cells and increased insulin secretion in db/db mice compared with DM group (P<0.05). Our results indicated that artemether significantly improved glucose homeostasis and insulin resistance and had the potential activity to prevent obesity, reduced the severity of fatty liver, and protected pancreatic beta cells, promising to treat type 2 diabetes.

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
I. N. Mefford ◽  
J. T. Mefford ◽  
C. A. Burris

A 43-year-old man with type 2 diabetes, opposed to insulin use and poorly responsive to oral agents added sequentially over 6 years, was placed on 40 mg omeprazole twice daily. A linear decline in daily fasting blood glucose was observed over the first two-month treatment, and his hemoglobin A1c was reduced from 11.9% to 8.2%, then sustained at 8.1% after four months. Glucose, insulin, and C-peptide response to a 2-hour glucose tolerance test were consistently improved across this time period, and calculated beta-cell mass increased by 67%. We believe these responses are consistent with activation or neogenesis of pancreatic beta cells, possibly through a gastrin-mediated mechanism.


2007 ◽  
Vol 98 (5) ◽  
pp. 929-936 ◽  
Author(s):  
Klaus Rave ◽  
Kerstin Roggen ◽  
Sibylle Dellweg ◽  
Tim Heise ◽  
Heike tom Dieck

Subjects with obesity and elevated fasting blood glucose are at high risk of developing type 2 diabetes which may be reduced by a dietary intervention leading to an improvement of insulin resistance. We investigated the potential of a whole-grain based dietary product (WG) with reduced starch content derived from double-fermented wheat during a hypo-energetic diet to positively influence body weight, fasting blood glucose, insulin resistance and lipids in comparison to a nutrient-dense meal replacement product (MR) in a randomized two-way cross-over study with two 4-week treatment periods separated by a 2-week wash-out. Subjects replaced at least two daily meals with WG and MR, respectively, targeting for a consumption of 200 g of either product per day. Total daily energy intake was limited to 7120 kJ. Thirty-one subjects (BMI 33·9 (sd 2·7) kg/m2, fasting blood glucose 6·3 (sd 0·8) mmol/l) completed the study. In both treatment groups body weight ( − 2·5 (sd 2·0) v. − 3·2 (sd 1·6) kg for WG v. MR), fasting blood glucose ( − 0·4 (sd 0·3) v. − 0·5 (sd 0·5) mmol/l), total cholesterol ( − 0·5 (sd 0·5) v. − 0·6 (sd 0·5) mmol/l), TAG ( − 0·3 (sd 0·9) v. − 0·3 (sd 1·2) mmol/l) and homeostasis model assessment (HOMA) insulin resistance score ( − 0·7 (sd 0·8) v. − 1·1 (sd 1·7) μU/ml ×  mmol/l) improved (P < 0·05) with no significant differences between the treatments. After statistical adjustment for the amount of body weight lost, however, the comparison between both groups revealed that fasting serum insulin (P = 0·031) and HOMA insulin resistance score (P = 0·049) improved better with WG than with MR. We conclude that WG favourably influences metabolic risk factors for type 2 diabetes independent from the amount of body weight lost during a hypo-energetic diet.


2014 ◽  
Vol 92 (8) ◽  
pp. 613-620 ◽  
Author(s):  
Joana Moitinho Oliveira ◽  
Sandra A. Rebuffat ◽  
Rosa Gasa ◽  
Ramon Gomis

Insulin receptor substrate 2 (IRS2) is a widely expressed protein that regulates crucial biological processes including glucose metabolism, protein synthesis, and cell survival. IRS2 is part of the insulin – insulin-like growth factor (IGF) signaling pathway and mediates the activation of the phosphotidylinositol 3-kinase (PI3K)–Akt and the Ras–mitogen-activated protein kinase (MAPK) cascades in insulin target tissues and in the pancreas. The best evidence of this is that systemic elimination of the Irs2 in mice (Irs2−/−) recapitulates the pathogenesis of type 2 diabetes (T2D), in that diabetes arises as a consequence of combined insulin resistance and beta-cell failure. Indeed, work using this knockout mouse has confirmed the importance of IRS2 in the control of glucose homeostasis and especially in the survival and function of pancreatic beta-cells. These studies have shown that IRS2 is critically required for beta-cell compensation in conditions of increased insulin demand. Importantly, islets isolated from T2D patients exhibit reduced IRS2 expression, which supports the likely contribution of altered IRS2-dependent signaling to beta-cell failure in human T2D. For all these reasons, the Irs2−/− mouse has been and will be essential for elucidating the inter-relationship between beta-cell function and insulin resistance, as well as to delineate therapeutic strategies to protect beta-cells during T2D progression.


2019 ◽  
Vol 2 (2) ◽  
pp. 61-66
Author(s):  
Yetty Machrina ◽  
Ambrocious Purba ◽  
Dharma Lindarto ◽  
Milahayati Daulay

Exercise is non-pharmacological management for Diabetes Mellitus (DM) type-2. Previous study found that both eerobic and interval training improved insulin resistance. The aim of this study was to analyze the chronic effect various type of exercises to fasting blood glucose (FBG) and insulin resistance in DM type-2 model rats. It was an experimental study, twenty male Wistar rats, age 8 weeks, weight 150-180 gram as the object. Rats were given high fed diet for 4 weeks then injected streptozocin dose 30 mg/kgBB in citrate buffer pH 4.5 i.p, and 45 mg/kgBB  at the following week. Groups were divided into i.e moderate continous training (MCT), severe continous training (SCT), slow interval training (SIT), and fast interval training (FIT). All groups were treated with ran on the treadmill three times a week for 8 weeks. Fasting blood glucose and fasting insulin were checked before and after intervention. Insulin resistance was determined by calculating HOMA-IR. Data analized with paired t-test (p<0,05). The results shown that all group significantly decreased fasting blood glucose and insulin resistance (p <0,05) after eight weeks exercise except insulin resistance in MCT group.  Fasting blood glucose and insulin resistence post-test was found lowest in SIT groups in this study.  In conclucions chronic effect of aerobic continous and aerobic interval in various intensity can decrease fasting blood glucose and insulin resistance in DM type-2 rat model. Slow interval training was the best exercise model to decrease insulin resistance.


2016 ◽  
Vol 38 (4) ◽  
pp. 155
Author(s):  
Elsi Kelana ◽  
Ellyza Nasrul ◽  
Rismawati Yaswir ◽  
Desywar Desywar

AbstrakResistensi insulin merupakan penurunan respons biologis jaringan terhadap insulin dalam kadar normal. Pada DM tipe 2 terjadi resistensi dan gangguan sekresi insulin. Terdapat indeks baru 20/(C-peptide puasa x glukosa darah puasa) untuk menilai resistensi sekaligus gangguan sekresi insulin. Penelitian bertujuan membuktikan korelasi indeks 20/(C-peptide puasa x glukosa darah puasa) dengan HOMA-IR untuk menilai resistensi insulin pada DM tipe 2 di RSUP. Dr. M. Djamil Padang. Dengan menggunakan sampel darah dari pasien, kadar glukosa darah puasa, insulin puasa dan C-peptide puasa ditentukan. Data yang diperoleh kemudian dianalisis menggunakan korelasi Pearson. Hasil penelitian menunjukkan rerata kadar glukosa puasa 9,83 (3,53) mmol/L [177 (63,54) mg/dL], insulin puasa 10,58 (3,61) μU/L, dan C-peptide puasa 0,97 (0,29) nmol/L dan terdapat korelasi yang sangat kuat dan bermakna secara statistik (p<0,0001) antara indeks 20/(C-peptide puasa x glukosa darah puasa) dengan HOMA-IR (r= -0,838). Dapat disimpulkan bahwa indeks 20/(C-peptide puasa x glukosa darah puasa) dan HOMA–IR berkorelasi kuat untuk menilai resistensi insulin pada DM tipe 2 di RSUP. Dr. M. Djamil Padang.AbstractInsulin resistance is a decrease of biological response of the tissues to the normal level of insulin. In type 2 diabetes, there is resistance and impaired of insulin secretion. There is a new index available to assess resistance and impaired of insulin secretion all at once, with the formula 20/(fasting C-peptide x fasting blood glucose). This study aimed to prove the correlation of this new index to the HOMA-IR (Homeostasis model assesment of insulin resistance) in type 2 diabetes at Dr.M.Djamil Padang hospital. Level of fasting glucose, fasting insulin and fasting C-peptide of blood were measured, followed by statistical data analysis using Pearson correlation test.The result showed the mean of fasting blood glucose, fasting insulin and fasting C-peptide were 9.83 (3.53) mmol/L[177 (63.54) mg/dl], 10.58 (3.61) μU/L, and 0.97 (0.29) nmol/L respectively.There was a strong and statistically significant correlation (p<0.0001) found between the new index and the HOMA-IR ( r= -0.838). To be concluded, the index 20/(fasting C-peptide x fasting blood glucose) and HOMA-IR was strongly correlated to assess insulin resistance in type 2 diabetes at Dr. M. Djamil Padang hospital.


2021 ◽  
pp. 21-27
Author(s):  
T. S. Vatseba

Abstract. The aim of the study was to investigate insulin resistance in patients with pancreatic and colorectal cancer diagnosed in people with type 2 diabetes. Materials and methods. 64 patients were examined. They were divided into the following groups: group I – healthy people (control group) (n = 16); group II – patients with type 2 diabetes without cancer (n = 28); group IIIa – patients with type 2 diabetes with pancreatic cancer (n = 10), group IIIb – patients with type 2 diabetes with colorectal cancer (n = 10). The study involved patients from specialized departments of the Ivano-Frankivsk Regional Hospital and the Precarpathian Clinical Oncology Center. Blood insulin levels were determined by enzyme-linked immunosorbent assay, using Insulin ELISA diagnostic kits, EIA-2935. Fasting blood glucose was determined by glucose oxidase method. Compensation for diabetes was assessed by the level of glycated hemoglobin (HbA1c) and determined by ion exchange chromatography. Data analysis was performed using Statistica 12.0 (StatSoft Inc., USA). Differences between the values in the comparison groups were determined by Student’s t-test and were considered significant at P < 0.05. Results. Patients with type 2 diabetes who were diagnosed with pancreatic cancer or colorectal cancer were older, compared with patients with type 2 diabetes without cancer (P < 0.05). Obesity was diagnosed in patients with colorectal cancer of group IIIb, their BMI was higher in comparison with patients of group IIIa who suffered from pancreatic cancer (P < 0.05). BMI in patients of group IIIa was lower than in control group (P < 0.05), in patients of group II (P < 0.05) and in patients of group IIIb with colorectal cancer (P < 0.05). Compared with patients of group II, patients with pancreatic and colorectal cancer had significantly lower insulin levels (P < 0.05), but significantly higher fasting blood glucose levels (P < 0.05). Insulin resistance according to the HOMA-IR index (> 3.0) was detected in both types of cancer. The HOMA-IR index in patients with pancreatic cancer was significantly lower than in patients of group II (P < 0.05). The level of HbA1c in patients with type 2 diabetes without cancer and in patients with cancer diagnosed on the background of diabetes did not differ significantly (P > 0.05). Prior to cancer detection, the same number of patients (50.0%) received metformin-free therapy in both the pancreatic cancer group and the colorectal cancer group. However, the duration of diabetes in patients with pancreatic cancer was 2.90 ± 2.60 years and was significantly shorter than in patients with colorectal cancer 9.70 ± 5.66 (P < 0.05). 80.0% of patients in group IIIa had a history of diabetes less than 5 years, and 80.0% of patients in group IIIb – more than 5 years. Conclusions: 1.In patients with type 2 diabetes mellitus with pancreatic cancer, as well as in patients with colorectal cancer, insulin resistance was detected by the HOMA-IR index, which depended on the combined effect of insulin and hyperglycemia in patients with colorectal cancer and on the fasting blood glucose in patients with pancreatic cancer. 2. The absence of hyperinsulinemia, the short duration of type 2 diabetes in patients with pancreatic cancer may be indirect evidence of cancer induced pancreatogenic diabetes (T3cDM) in the majority of patients of this group. For elderly patients with newly diagnosed diabetes mellitus without obesity, without hyperinsulinemia, screening for pancreatic cancer is recommended.


2010 ◽  
Vol 13 (3) ◽  
pp. 62-65 ◽  
Author(s):  
Alexander Sergeevich Ametov ◽  
Elena Nikolaevna Pakus

Aim. To elucidate therapeutic effect of metformin-sitaglitin combination on the dynamics of indices of insulin resistance and functional activity of pancreaticbeta-cells, lipid metabolism and body weight in patients with type 2 diabetes mellitus (DM2) and obesity. Materials and methods. The study included 32 patients treated by a combination of metformin (500-2550 mg/day) and sitagliptin (100 mg) for18 weeks. Standard parameters of carbohydrate and lipid metabolism, body mass index (BMI), blood adiponectin and leptin levels were measured, indices of insulin resistance and functional activity of pancreatic beta-cells were calculated. Results. Therapy with metformin-sitagliptin combination ensured compensation of fasting and postprandial hyperglycemia, reduced HbA1c level, increasedfunctional activity of beta-cells, decreased peripheral insulin resistance and BMI, had beneficial effect on lipid metabolism and hormonalactivity of adipose tissue. Conclusion. Metformin-sitagliptin combination can be recommended as a clinically efficacious modality for the treatment of patients with diabetesmellitus and obesity.


2022 ◽  
Vol 28 (1) ◽  
pp. 59-61
Author(s):  
Bin Zhang

ABSTRACT Introduction: Type 2 diabetes mellitus (T2DM), also known as non-insulin-dependent diabetes mellitus (NIDDM), accounts for more than 90% of the total number of diabetes mellitus cases and often occurs in middle-aged and elderly people. Objective: To investigate the effect of exercise intervention on insulin resistance in obese type 2 diabetes patients. Methods: Eighty-six obese diabetic patients were screened as experimental subjects in physical examinations and randomly divided into observation and control groups. Visceral fat volume, fasting blood glucose, and fasting insulin of all subjects were measured before and after completion of the 6-month experimental implementation. The insulin resistance was calculated for both groups and the values for each indicator were compared statistically between groups. Results: Control of body weight, body mass index, blood glucose, blood lipids and insulin resistance index were better in the observation group than in the control group, and the difference was statistically significant (P < 0.05). Conclusions: Basal intervention with quantitative exercise can significantly improve insulin resistance in obese type 2 diabetes patients and the effect is better than treatment with diet and conventional exercise. Level of evidence II; Therapeutic studies - investigation of treatment results.


2017 ◽  
Vol 53 (1) ◽  
pp. 12 ◽  
Author(s):  
Dewa Ayu Agung Alit Suka Astini ◽  
H Ari Gunawan ◽  
R Mochamad Wirono Aman Santoso ◽  
Susilowati Andajani ◽  
Ahmad Basori

Based on some researches known that soursop leaf extract can improve beta cell injury. The aims of this study was to analyze the effect of soursop leaf extract on fasting blood glucose (FBG) and pancreatic beta cell number in male Wistar rats wich were exposed to a high-fat diet and streptozotocin. This study design is the only randomized posttest control group design. The total sample size is 50 male Wistar rats. The independent variable: high-fat diet, STZ, and soursop leaf extract; the dependent variable: pancreatic beta cells number, and FBG3. Data tested for normality with Kolmogorov-Smirnov (a=0.05) and tested of homogeneity with Levene (a =0.05). Comparison test between groups with Kruskal-Wallis (a=0.05), followed by Mann Whitney. Correlation test with Pearson (a=0.05) between dose of the soursop leaf extract and FBG3, and between dose and the number of pancreatic beta cells. The results of this study showed that the soursop leaf extract at a dose of 100 mg/kg and 150 mg/kg have an effect on fasting blood glucose levels and panreatic beta cells number;2)There is a significant negative correlation between the orograstric lavage of soursop leaf extract with FBG3 (r=-0.647;p<0.001), the increasing doses of soursop leaf extract, further lowering fasting blood glucose levels;3)There is a significant positive correlation between the orograstric lavage of soursop leaf extract with the number of pancreatic beta cells (r=0,759;p<0,001), the increasing doses of soursop leaf extract, further increasing pancreatic beta cells number. In conclusion, increasing doses of soursop leaf extract, further lowering fasting blood glucose and increasing the number of pancreatic beta cells.


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