Actos (pioglitazone)

Title: Actos (pioglitazone)
Category: Medications
Created: 11/28/1999 12:00:00 AM
Last Editorial Review: 11/1/2016 12:00:00 AM

Source MedicineNet Diabetes General http://ift.tt/2cTOxlY

Health Tip: Snacking Healthier With Diabetes

Title: Health Tip: Snacking Healthier With Diabetes
Category: Health News
Created: 11/1/2016 12:00:00 AM
Last Editorial Review: 11/1/2016 12:00:00 AM

Source MedicineNet Diabetes General http://ift.tt/2eyfbwm

glucagon (recombinant - GlucaGen, Glucagon Emergency Kit)

Title: glucagon (recombinant - GlucaGen, Glucagon Emergency Kit)
Category: Medications
Created: 6/21/2001 12:00:00 AM
Last Editorial Review: 10/31/2016 12:00:00 AM

Source MedicineNet Diabetes General http://ift.tt/2e0I747

Keeping Healthy is a Family Affair

You and your family can work together to create a road map to lower your risks for diabetes, health disease and other health problems.

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New Guidelines Urge Diabetics to Move More

Title: New Guidelines Urge Diabetics to Move More
Category: Health News
Created: 10/26/2016 12:00:00 AM
Last Editorial Review: 10/27/2016 12:00:00 AM

Source MedicineNet Diabetes General http://ift.tt/2eh1bqC

Renal Denervation Reverses Hepatic Insulin Resistance Induced by High-Fat Diet

Activation of the sympathetic nervous system (SNS) constitutes a putative mechanism of obesity-induced insulin resistance. Thus, we hypothesized that inhibiting the SNS by using renal denervation (RDN) will improve insulin sensitivity (S_I) in a nonhypertensive obese canine model. S_I was measured using euglycemic-hyperinsulinemic clamp (EGC), before (week 0 [w0]) and after 6 weeks of high-fat diet (w6-HFD) feeding and after either RDN (HFD + RDN) or sham surgery (HFD + sham). As expected, HFD induced insulin resistance in the liver (sham 2.5 ± 0.6 vs. 0.7 ± 0.6 x 10^–4 dL ⋅ kg^–1 ⋅ min^–1 ⋅ pmol/L^–1 at w0 vs. w6-HFD [P < 0.05], respectively; HFD + RDN 1.6 ± 0.3 vs. 0.5 ± 0.3 x 10^–4 dL ⋅ kg^–1 ⋅ min^–1 ⋅ pmol/L^–1 at w0 vs. w6-HFD [P < 0.001], respectively). In sham animals, this insulin resistance persisted, yet RDN completely normalized hepatic S_I in HFD-fed animals (1.8 ± 0.3 x 10^–4 dL ⋅ kg^–1 ⋅ min^–1 ⋅ pmol/L^–1 at HFD + RDN [P < 0.001] vs. w6-HFD, [P not significant] vs. w0) by reducing hepatic gluconeogenic genes, including G6Pase, PEPCK, and FOXO1. The data suggest that RDN downregulated hepatic gluconeogenesis primarily by upregulating liver X receptor α through the natriuretic peptide pathway. In conclusion, bilateral RDN completely normalizes hepatic S_I in obese canines. These preclinical data implicate a novel mechanistic role for the renal nerves in the regulation of insulin action specifically at the level of the liver and show that the renal nerves constitute a new therapeutic target to counteract insulin resistance.

Source Diabetes Pathophysiology http://ift.tt/2er8TUG

Metabolic Aberrations Impact Biophysical Integrity of Macromolecular Protein Pools in the Default Mode Network

The brain’s default mode network (DMN), having a high rate of basal energy metabolism, is vulnerable to altered glucose metabolism in type 2 diabetes mellitus (T2DM) due to insulin resistance and chronic hyperglycemia. Previous studies showed that functional connectivity and structural connectivity among the DMN nodal regions are compromised in T2DM. We applied magnetization transfer imaging to examine the impact of T2DM on the biophysical integrity of the DMN. The results showed that the biophysical integrity of macromolecular protein pools in the posterior cingulate cortex (PCC), a central DMN hub region, was selectively compromised in T2DM, whereas the other nodal regions of the DMN, including the medial prefrontal cortex, lateral inferior parietal cortex, precuneus, and medial and lateral temporal cortices, were biophysically intact compared with those of control subjects without diabetes. Furthermore, the degree of biophysical impairment of the PCC correlated with both hyperglycemia and vascular compromise, the two physiological hallmarks of diabetes. These new findings demonstrate that the PCC is vulnerable in the DMN and may shed light on the molecular neurobiology of T2DM and help to elucidate the pathophysiology of diabetes-related cognitive comorbidities and increased risk for dementia.

Source Diabetes Pathophysiology http://ift.tt/2eG0Lwc