First Record of <Emphasis Type="Italic">Euphoria lurida</Emphasis> Fabricius (Coleoptera: Scarabaeidae) Injurious to Safflower (<Emphasis Type="Italic">Carthamus tinctorius</Emphasis> L.) (Asterales: Asteraceae) in Brazil

We present the first report on Euphoria lurida (Fabricius) (Coleoptera: Scarabaeidae) infestation on safflower (Carthamus tinctorius L.), a crop of industrial and medicinal importance. Between September and October 2013–2015 in Paraná State, we observed E. lurida adults feeding on safflower plants from the inception of flower head formation onwards, over an area of approximately 400 m². Losses in the productivity of infested plants were estimated between 15 and 50%. The damage was characterized by perforations in the upper portion and at the base of the developing flower heads or open flowers, resulting in withering and abortion of the reproductive structures.     

The role of glucose metabolism and insulin resistance in cardiac remodelling induced by cigarette smoke exposure

The aim of this study is to evaluate whether the alterations in glucose metabolism and insulin resistance are mechanisms presented in cardiac remodelling induced by the toxicity of cigarette smoke. Male Wistar rats were assigned to the control group (C; n = 12) and the cigarette smoke-exposed group (exposed to cigarette smoke over 2 months) (CS; n = 12). Transthoracic echocardiography, blood pressure assessment, serum biochemical analyses for catecholamines and cotinine, energy metabolism enzymes activities assay; HOMA index (homeostatic model assessment); immunohistochemistry; and Western blot for proteins involved in energy metabolism were performed. The CS group presented concentric hypertrophy, systolic and diastolic dysfunction, and higher oxidative stress. It was observed changes in energy metabolism, characterized by a higher HOMA index, lower concentration of GLUT4 (glucose transporter 4) and lower 3-hydroxyl-CoA dehydrogenase activity, suggesting the presence of insulin resistance. Yet, the cardiac glycogen was depleted, phosphofructokinase (PFK) and lactate dehydrogenase (LDH) increased, with normal pyruvate dehydrogenase (PDH) activity. The activity of citrate synthase, mitochondrial complexes and ATP synthase (adenosine triphosphate synthase) decreased and the expression of Sirtuin 1 (SIRT1) increased. In conclusion, exposure to cigarette smoke induces cardiac remodelling and dysfunction. The mitochondrial dysfunction and heart damage induced by cigarette smoke exposure are associated with insulin resistance and glucose metabolism changes.