Rapid development of cardiac dysfunction in a canine model of insulin resistance and moderate obesity.

AIMS/HYPOTHESIS: The worldwide incidence of obesity and diabetes continues to rise at an alarming rate. A major cause of the morbidity and mortality associated with obesity and diabetes is heart disease, yet the mechanisms that lead to cardiovascular complications remain unclear. METHODS: We performed cardiac MRI to assess left ventricular morphology and function during the development of moderate obesity and insulin resistance in a well-established canine model (n = 26). To assess the influence of dietary fat composition, we randomised animals to a traditional lard diet (rich in saturated and monounsaturated fat; n = 12), a salmon oil diet (rich in polyunsaturated fat; n = 8) or a control diet (n = 6). RESULTS: High-fat feeding with lard increased body weight and fasting insulin and markedly reduced insulin sensitivity. Lard feeding also significantly reduced left ventricular function, evidenced by a worsening of circumferential strain and impairment in left ventricular torsion. High-fat feeding with salmon oil increased body weight; however, salmon oil feeding did not impair insulin sensitivity or cardiac function. CONCLUSIONS/INTERPRETATION: These data emphasise the importance of dietary fat composition on both metabolic and cardiac function, and have important implications for the relationship between diet and health.

Hepatic portal vein denervation impairs oral glucose tolerance but not exenatide's effect on glycemia.

The hepatoportal area is an important glucohomeostatic metabolic sensor, sensing hypoglycemia, hyperglycemia, and hormones such as glucagon-like peptide-1 (GLP-1). We have reported previously that activation of hepatoportal sensors by intraportal infusion of glucose and GLP-1 or by subcutaneous administration of GLP-1 receptor activator exenatide and of intraportal glucose improved glycemia independent of corresponding changes in pancreatic hormones. It is not clear whether this effect is mediated via the portal vein (PV) or by direct action on the liver itself. To test whether receptors in the PV mediate exenatide's beneficial effect on glucose tolerance, we performed 1) paired oral glucose tolerance tests (OGTT) with and without exenatide and 2) intravenous glucose tolerance tests before and after PV denervation in canines. Denervation of the portal vein affected oral glucose tolerance; post-denervation (POST-DEN) OGTT glucose and insulin AUC were 50% higher than before denervation (P = 0.01). However, portal denervation did not impair exenatide's effect to improve oral glucose tolerance (exenatide effect: 48 ± 12 mmol·l⁻¹·min before vs. 64 ± 26 mmol·l⁻¹·min after, P = 0.67). There were no changes in insulin sensitivity or secretion during IVGTTs. Portal vein sensing might play a role in controlling oral glucose tolerance during physiological conditions but not in pharmacological activation of GLP-1 receptors by exenatide.

The effect of innovation on CO2 emissions of OCED countries from 1990 to 2014.

Human activities are accelerating CO2 emissions all over the world most especially in high-income nations, spurring the rise in greenhouse gas emissions. For decades, technologies have been developed and patented in response to the environmental problems. There is an outcry for innovative ways to combat the environmental menace. This attests to the enormity of research being done, in recent years, to investigate how innovation can help mitigate CO2 emissions. This research aims at investigating into the effect of innovation on CO2 emissions in 28 OCED countries at an individual level for the recent period 1990 to 2014. The source of data for our utilized variables is the World Bank Indicators. Our study employed three key models based on the STIRPAT model, the economic-EKC growth model, and the innovation-EKC model. The findings of our study revealed that innovation plays a key role towards mitigation of CO2 emissions in most OECD countries. Its impact, however, varies across the countries, depending on some key factors and channels elucidated in this paper. Additionally, our study asserts that improvement in GDP per capita leads to the rise in CO2 in most OECD economies, although mitigate emissions in few OECDs; hence, the economic-EKC model is not valid for most economies. Non-renewable energy accelerates emissions whiles renewable energy sources mitigate emissions. Research and development (R&D) improves environmental quality and the EKC for both economic growth and innovation, valid for a few economies of the OECDs. We conclude that innovation is necessary in mitigating CO2 emissions; hence, governments and policy makers should invest and promote innovative renewable energy sources.

Insulin Access to Skeletal Muscle is Preserved in Obesity Induced by Polyunsaturated Diet.

OBJECTIVE: Diets high in saturated fat induce obesity and insulin resistance and impair insulin access to skeletal muscle, leading to reduced insulin levels at the muscle cell surface available to bind insulin receptors and induce glucose uptake. In contrast, diets supplemented with polyunsaturated fat improve insulin sensitivity (SI) and reduce the risk for type 2 diabetes. It was hypothesized that a diet high in polyunsaturated fat would preserve SI and insulin access to muscle, as compared with a diet high in saturated fat. METHODS: After 12 weeks of control, saturated (LARD), or polyunsaturated (salmon oil [SO]) high-fat diet feeding, muscle SI and insulin access to skeletal muscle were measured by using lymph, a surrogate of skeletal muscle interstitial fluid. RESULTS: Both high-fat diets induced similar weight gain, yet only LARD impaired SI. Hyperinsulinemia in the LARD group did not induce an increase in basal interstitial insulin, suggesting reduced insulin access to muscle after LARD, but not after SO. CONCLUSIONS: A diet high in polyunsaturated fat does not impair insulin access to muscle interstitium or induce insulin resistance as observed with a saturated fat diet, despite similar weight gain. Future studies should determine whether dietary SO supplementation improves impairments in insulin access to skeletal muscle.

Carbon dioxide emission and economic growth of China-the role of international trade.

This study investigates the role of international trade in mitigating carbon dioxide emission as a nation economically advances. This study disaggregated the international trade into total exports and total imports. A multivariate model framework was estimated for the time series data for the period of 1970-2014. The quantile regression detected all the essential relationship, which hitherto, the traditional ordinary least squares could not capture. A cointegration relationship was confirmed using the Johansen cointegration model. The findings of the Granger causality revealed the presence of a uni-directional Granger causality running from energy consumption to economic growth; from import to economic growth; from imports to exports; and from urbanisation to economic growth, exports and imports. Our study established the presence of long-run relationships amongst carbon dioxide emission, economic growth, energy consumption, imports, exports and urbanisation. A bootstrap method was further utilised to reassess the evidence of the Granger causality, of which the results affirmed the Granger causality in the long run. This study confirmed a long-run N-shaped relationship between economic growth and carbon emission, under the estimated cubic environmental Kuznet curve framework, from the perspective of China. The recommendation therefore is that China as export leader should transform its trade growth mode by reducing the level of carbon dioxide emission and strengthening its international cooperation as it embraces more environmental protectionisms.

Insulin access to skeletal muscle is impaired during the early stages of diet-induced obesity.

OBJECTIVE: Insulin must move from the blood to the interstitium to initiate signaling, yet access to the interstitium may be impaired in cases of insulin resistance, such as obesity. This study investigated whether consuming a short- and long-term high-fat diet (HFD) impairs insulin access to skeletal muscle, the major site of insulin-mediated glucose uptake. METHODS: Male mongrel dogs were divided into three groups consisting of control diet (n = 16), short-term (n = 8), and long-term HFD (n = 8). Insulin sensitivity was measured with intravenous glucose tolerance tests. A hyperinsulinemic euglycemic clamp was performed in each animal at the conclusion of the study. During the clamp, lymph fluid was measured as a representation of the interstitial space to assess insulin access to muscle. RESULTS: Short- and long-term HFD induced obesity and reduced insulin sensitivity. Lymph insulin concentrations were approximately 50% of plasma insulin concentrations under control conditions. Long-term HFD caused fasting plasma hyperinsulinemia; however, interstitial insulin concentrations were not increased, suggesting impaired insulin access to muscle. CONCLUSIONS: A HFD rapidly induces insulin resistance at the muscle and impairs insulin access under basal insulin concentrations. Hyperinsulinemia induced by a long-term HFD may be a compensatory mechanism necessary to maintain healthy insulin levels in muscle interstitium.