Insulin resistance: Review of the underlying molecular mechanisms.

Most human cells utilize glucose as the primary substrate, cellular uptake requiring insulin. Insulin signaling is therefore critical for these tissues. However, decrease in insulin sensitivity due to the disruption of various molecular pathways causes insulin resistance (IR). IR underpins many metabolic disorders such as type 2 diabetes and metabolic syndrome, impairments in insulin signaling disrupting entry of glucose into the adipocytes, and skeletal muscle cells. Although the exact underlying cause of IR has not been fully elucidated, a number of major mechanisms, including oxidative stress, inflammation, insulin receptor mutations, endoplasmic reticulum stress, and mitochondrial dysfunction have been suggested. In this review, we consider the role these cellular mechanisms play in the development of IR.

The Effects of Glucagon-Like Peptide-1 Receptor Agonists and Dipeptydilpeptidase-4 Inhibitors on Blood Pressure and Cardiovascular Complications in Diabetes.

Glucagon-like peptide-1 receptor (GLP-1R) agonists are a class of newly introduced antidiabetic medications that potentially lower blood glucose by several molecular pathways. DPP-4 inhibitors are the other type of novel antidiabetic medications which act by preventing GLP-1 inactivation and thereby increasing the activity levels of GLP-1, leading to more glucose-induced insulin release from islet ß-cells and suppression of glucagon release. Most patients with diabetes have concurrent hypertension and cardiovascular disorder. If antihyperglycemic agents can attenuate the risk of hypertension and cardiovascular disease, they will amplify their overall beneficial effects. There is conflicting evidence on the cardiovascular benefits of GLP-1R induction in laboratory studies and clinical trials. In this study, we have reviewed the main molecular mechanisms by which GLP-1R induction may modulate the cardiovascular function and the results of cardiovascular outcome clinical trials.

Outcome of Acute Kidney Injury in Critical Care Unit, Based on AKI Network.

BACKGROUND: Acute Kidney Injury (AKI) is an unsolved clinical problem in critical care patients with a high mortality rate, increasing incidence, and no definitive therapy. We studied the incidence, risk factors, and mortality associated with AKI in ICU patients. MATERIALS AND METHODS: In a prospective study, patient demographics, reason for hospitalization, reason for ICU admission, Length of ICU stay, laboratory data, and Vital signs were recorded in prepared forms during the ICU stay. AKI was defined as an increase in serum creatinine (SCr) of ≥ 0.3mg/dl from the baseline. RESULTS: A total of 200 patients who were enrolled in our study; 134 (67%) did not develop AKI during their ICU stay while 66 (33%) developed AKI (SCr ≥ 0.3) according to the AKIN definition. Patients with AKI had higher APACHE II scores (12.3±5.6 vs. 6.9±3.6; P< 0.001), longer ICU stays (7.6±7.6 vs. 3.7±2.8 days respectively; P< 0.001), and higher mortality (19.7% vs. 0.7%; P< 0.001). CONCLUSION: The AKIN criteria are clinically valid and can be a good predictor of mortality and patient outcome in addition to APACHE II score in ICU patients.