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et al. 2009 ). The purpose of this review is to highlight how SMKIs that are often designed for cancer treatment can alter blood glucose and insulin. We apologize that not all relevant literature could be included in this review. We selected specific

Introduction Islet dysfunction in type 2 diabetes is bi-hormonal involving both defective insulin secretion and augmented glucagon secretion ( Unger & Orci 1975 ), the latter resulting in chronic elevation of circulating glucagon levels ( Larsson

, reflected by the presence of pancreatic autoantibodies in the blood ( Regnell & Lernmark 2017 ). Identification of such antibodies in plasma or serum is a strong indicator that the patient will eventually need insulin treatment to maintain glucose

rapidly regulated by insulin ( Uldry & Thorens 2004 ). In CL of dogs, our group has demonstrated a differential expression of glucose transporter 1 ( SLC2A1 /GLUT1), which accompanied hypoxia during the cycle ( Papa et al . 2014 ), pointing out that the

by the release of the pancreatic hormones insulin and glucagon. These hormones target metabolically active tissues such as muscle, adipose tissue and liver in order to maintain blood glucose concentration within narrow limits (∼4.0–6.0 mmol

2015). Obesity is defined as excess accumulation of body fat or adipose tissue and is considered to be the antecedent of metabolic disorders such as insulin resistance (IR), type 2 diabetes, hypertension, dyslipidemia, cardiovascular diseases, etc. ( Ye

/db ) animals ( Bray & York 1979 ). Numerous studies report that insulin increases leptin production and secretion from adipose tissue in rodents ( Cusin et al. 1995 , Barr et al. 1997 , Koopmans et al. 1998 ), while Kieffer et al. (1996

Introduction Obesity and the metabolic syndrome are associated with insulin resistance, hyperinsulinaemia, type 2 diabetes mellitus (T2DM) and serious cardiovascular sequelae ( Eckel et al . 2005 ). Adipose tissue produces cytokines termed

Introduction EC 3.4.11.3 protein (IRAP, insulin-regulated aminopeptidase), also known as vp165, GP160 ( Keller 2004 ), placental leucine aminopeptidase (AP) ( Mizutani et al . 2011 ), cystyl AP, oxytocinase ( Rogi et al . 1996 ), and angiotensin

of leptin, insulin, non-esterified free fatty acids (NEFAs), and glucose in mice. Measures were collected from mice maintained on a standard diet or high-fat diet (HFD). Correlation analyses confirmed an inverse relationship between measures of