جستجوی مقالات مرتبط با کلیدواژه "hyperinsulinemia" در نشریات گروه "پزشکی"

Pregnancy is a diabetogenic state characterized by hyperinsulinemia and insulin resistance. The primary goal of identifying gestational diabetes mellitus (GDM) is to detect women at risk for adverse perinatal outcomes. Proper diagnosis of this condition and its complications is essential for the benefit of both maternal and child health. The uric acid/HDL-C ratio (UHR), which combines two metabolic parameters—serum uric acid and HDL-C— is a powerful predictor of metabolic deterioration. The present study aims to understand the role of metabolic derangement in the development of GDM in pregnant women and to compare these findings with those of healthy controls. The objectives of the study are to compare the serum UHR in the GDM and control populations and to correlate UHR in each group with glycemic status markers and BMI.

Based on inclusion and exclusion criteria, a total of 30 cases and 30 age-matched controls were selected for the study. The age range was 18 to 35 years. All serum parameters were analyzed using a Beckman Coulter AU-480 fully automated analyser. UHR was calculated from serum uric acid and HDL-C values using the formula: UHR = UA/HDL-C.

The results show that patients with GDM had higher uric acid levels and UHR and lower HDL-C levels than healthy controls, suggesting significant metabolic derangement in this group.

Routine use of UHR as an early screening tool can help identify metabolic abnormalities in GDM. This will also aid in early pharmacological intervention, thereby preventing future complications for both the mother and foetus.

Yam bean (Pachyrhizus erosus) is a potent medicinal plant exerting therapeutical effects against diseases. However, investigations on the health benefits of its fiber remain limited. This study aimed to investigate the potential of yam bean fiber (YBF) against a high-fat diet (HFD)-induced metabolic diseases, inflammation, and gut dysbiosis.

Adult male mice were assigned to four groups (8 each), namely a normal diet-fed group (ND), HFD-fed group, and HFD supplemented with YBF groups (HFD + YBF) at a dose of 2.5% and 10%, respectively. Treatments were implemented for ten weeks. Thereafter, indicators of metabolic diseases, oxidative stress, inflammation, and gut microbiota composition were determined.

A dosage of 10% YBF significantly inhibited excessive body weight gain (2.3 times lower than HFD group) and white adipose tissue (WAT) mass (2.2 times lower than HFD group) while sustaining brown adipose tissue mass. YBF prevented malondialdehyde elevation, catalase activity reduction, and expression of the interleukin-6 increment (2.7 times lower than the HFD group) within the WAT. Furthermore, YBF sustained normoglycaemia, glucose tolerance, and insulin sensitivity while precluding hyperinsulinemia. YBF modulated the gut microbiota community by increasing health-promoting microbiota including Lactobacillus reuteri, L. johnsonii, and inhibiting a pathogenic Mucispirillum sp. YBF prevented histopathology and inflammation of the colon.

 YBF at the dose of 10% is proved to be useful in the prevention of diet-induced metabolic diseases, microbiota dysbiosis, and inflammation. Hence, YBF is recommended as a potential natural-based remedy to diminish the detrimental effects of high-fat foods.

Most people with diabetes suffer from cardiovascular problems; however, increased oxidative stress caused by diabetes can increase the risk of DNA damage and cancer. Carvedilol is a third-generation beta-blocker that can both improve heart function and prevent oxidative stress.

The present study aimed to assess carvedilol’s genoprotective effects against hyperinsulinemia-induced DNA strand break in rats.

To evaluate the extent of DNA damage caused by high insulin concentrations and the effect of carvedilol on these lesions, isolated lymphocytes of high-fat type 2 diabetic rats were evaluated using the comet method.

Our results in this study using the comet method showed that hyperinsulinemia and hyperglycemia of high-fat diet have significant genotoxic parameters in rats (tail length 84.35 ± 0.23 vs. 0.90 ± 0.02, % DNA in tail 16.09 ± 0.09 vs. 7.63 ± 0.04, and tail moment 13.58 ± 0.09 vs. 0.07 ± 0.01) compared with the control group (P < 0.001). In rats receiving carvedilol, we observed the genoprotective effect in a dose-dependent manner, which is predicted due to the antioxidant activity of carvedilol and its metabolites.

It does not have an adverse effect on the blood sugar profile of diabetics and reduction of cardiovascular complications of the disease; carvedilol can prevent genetic damage and cancer risk in hyperinsulinemia induced by the high-fat diet.

Using a rat model of hyperinsulinemia, the present study investigated the role of p-ERK1/2 in benign prostatic hyperplasia (BPH).

Forty male Sprague-Dawley rats were randomly selected and assigned to four groups: high fat diet (HFD)+BPH (n=10), HFD (n=10), BPH (n=10), and control (n=10) groups. Hyperinsulinemia was in-duced by HFD feeding, while BPH was induced using testosterone propionate. Plasma glucose, plasma insulin and bodyweight were examined weekly. Immunohistochemistry (IHC) and western blot analysis were used to analyze the expression of ERK1/2 and p-ERK1/2 in rat prostates.

Plasma glucose and plasma insulin levels were significantly greater in the HFD+BPH and HFD groups, when compared to the other two groups (P < 0.05). Prostate weights were significantly greater in the HFD+BPH, HFD and BPH groups, than in the control group (P < 0.05). IHC and western blot analysis revealed that p-ERK1/2 expression was greater in the HFD+BPH group than in the other three groups (P < 0.05).

Androgens plus a hyperinsulinemic condition induced by HFD can result in prostatic cell hyperplasia, and this mechanism may be correlated to the upregulation of p-ERK1/2. Further investigations of this possibility are required.

Diabetes mellitus (DM) is known as a major public health issue worldwide. Type 2 diabetes does not have a clear inheritance pattern, although many affected people have at least one close family member, such as a parent or sibling, who is affected with the disease. The KCNJ11 gene is a member of the potassium channel gene family. Polymorphisms in KCNJ11 (E23K, rs5219) result in neonatal diabetes and congenital hyperinsulinemia, which are associated with diabetes susceptibility where the K allele plays an important role in insulin secretion. This study evaluates the frequency of these polymorphisms in 85 Kurdish patients with type 2 diabetes. E23K polymorphism was genotyped by the PCRRFLP method. Heterozygous carriers for AG are more in non-diabetic patients (P = 0.034).

Resveratrol (RSV) provides several important biological functions in wide variety of cells. In this study, we investigated the molecular mechanisms underlying anti-inflammatory effect of RSV on HepG2 cells by assessing the gene expression of RelA and c-Jun- subunits of NF-κB and AP-1 transcription factors.

HepG2 cells were settled in a serum- free medium with high concentrations of glucose (30 mM) and insulin (1 µM) overnight and were then incubated with RSV (5, 10, and 20 µM) for 24 and 48 hours. Real time quantitative polymerase chain reaction (qRT-PCR) was used to determine RelA and c-Jun expression.

RSV diminished hyperglycemia/hyperinsulinemia stimulated expression of c-Jun dose- dependently after 24 and 48 hours (p The findings of the present study demonstrated that RSV may be considered as a preventative and therapeutic agent for antagonizing inflammation in Hepatocellular carcinoma (HCC).

Prostate cancer (PCa) is the most common type of cancer among men over 60 years old. The aggressiveness and mortality of PCa can be correlated with obesity. Adipose tissue-derived cytokines such as adiponectin may explain the correlation between PCa and obesity. Since the correlation between adiponectin and aggressive PCa is still not fully evaluated, we aimed to investigate the probable role of adiponectin in PCa. Adiponectin is considered as a link between obesity, insulin resistance and diabetes. On the other hand, adiponectin is a key mediator of systemic insulin sensitivity and glucose homeostasis. Moreover, low level of adiponectin is associated with inflammation and angiogenesis. These processes could promote tumor growth. Special effects of adiponectin are mediated via adenosine monophosphate-activated protein kinase (AMPK). AMPK activation inhibits growth of androgen-independent and androgen-sensitive PCa cell lines. Moreover, c-Jun N-terminal protein kinase (JNK) and Signal transducer and activator of transcription 3 (STAT3) signaling pathway are known as adiponectin’s mediators on the metabolic syndrome and cancer. Furthermore, adiponectin acts as a tumor suppressor gene via inhibition of Epithelial-to-mesenchymal Transition (EMT) of PCa cells, but it is down regulated through hypermethylation of promoter gene in PCa cells. Therefore, according to the results of these studies, decreased concentration of adiponectin was associated with increased risk of PCa. It seems that hypoadiponectinemia may act as a promising biomarker for detection and diagnosis of PCa.

Epidemiological evidence shows that cancer and diabetes are major causes of death in the world. Type2 diabetes increases the risk of cancer-specific mortality. This review relates dia­betic therapies, diabetes and cancer. All published papers in this field were searched, looking into such databases as Science Direct, ISI Web of Knowledge, PubMed and Scopus. In cancer patients, metformin improves patient outcome and reduces cancer risk. Sulfonylureas may increase risk of cancer, but decreased risk of cancer is associated with thiazolidinediones in type2 diabetic subjects. Metformin lowers circulating insulin and it may be important for treatment of hyperinsulinemia-associated cancers, such as colon and breast cancer. However, laboratory investigations and large-scale population based studies are required for further investigation of association of cancer-preventive, anti-cancer and cancer-mortality of noninsulin antidiabetics.

Context: Turmeric is obtained from the plant Curcuma longa L; its major constituent, curcumin, is a polyphenol with multiple effects which can modulate some signaling pathways..Evidence Acquisition: Insulin resistance is a major risk factor for chronic diseases such as type 2 diabetes, atherosclerotic, metabolic syndrome and cardiovascular disease. In addition, Insulin resistance in peripheral tissue is one of the most important reasons of hyperglycemia which can cause global or systemic effects. The present study reviewed studies published in PubMed from 1998 to 2013, indicating the role of curcumin in attenuation of many pathophysiological processes involved in development and progression of hyperglycemia and insulin resistance.. Curcumin can reduce blood glucose level by reducing the hepatic glucose production, suppression of hyperglycemia-induced inflammatory state, stimulation of glucose uptake by up-regulation of GLUT4, GLUT2 and GLUT3 genes expressions, activation of AMP kinase, promoting the PPAR ligand-binding activity, stimulation of insulin secretion from pancreatic tissues, improvement in pancreatic cell function, and reduction of insulin resistance.. Curcumin has antihyperglycemic and insulin sensitizer effects. Thereby, more studies evaluating the effects of curcumin on hyperglycemic state and insulin resistance in related disorders such as diabetes are recommended..