Diabetes mellitus comprises a group of metabolic disorders characterized by elevated blood glucose levels resulting from defects in insulin secretion, insulin action, or both. The close relationship between metabolism and diabetes is well-established, with both type 1 and type 2 diabetes being metabolic diseases. Insulin, a hormone produced by the beta cells of the pancreas, plays a central role in glucose metabolism. In response to increased blood glucose levels, insulin is released to facilitate the uptake of glucose into cells, where it is used for energy production or stored as glycogen in the liver and muscles. Insulin also suppresses glucose production in the liver, helping to maintain blood glucose levels within a narrow range. Type 1 (insulin-dependent) diabetes results from an autoimmune attack on pancreatic beta cells, leading to a lack of insulin production. Without sufficient insulin, glucose cannot enter cells sufficiently, resulting in high blood glucose levels. Individuals with type 1 diabetes require lifelong insulin therapy to manage their blood glucose levels and prevent complications. Type 2 diabetes, the more common form of diabetes, is characterized by insulin resistance, where cells become increasingly less responsive to the effects of insulin. As a result, more insulin is required to facilitate equivalent glucose uptake into cells, initially leading to hyperinsulinemia (elevated insulin levels). Over time, the beta cells may become exhausted, leading to reduced insulin production, and further exacerbating hyperglycaemia. Glucose homeostasis is tightly regulated through a complex interplay of hormones. Apart from insulin, other hormones, such as glucagon, cortisol, and growth hormone, also influence blood glucose levels. Glucagon, produced by the pancreatic alpha cells, raises blood glucose levels by promoting glycogen breakdown in the liver (glycogenolysis) and stimulating glucose production (gluconeogenesis), whilst cortisol and growth hormone oppose the effects of insulin, leading to increased blood glucose levels. Adipose tissue, or fat, is an important player in diabetes and metabolism. Adipocytes release adipokines, such as adiponectin and leptin, which influence insulin sensitivity and appetite regulation. In obesity, excessive adipose tissue deposition can lead to insulin resistance and chronic low-grade inflammation, contributing to the development of type 2 diabetes. Additionally, in type 2 diabetes, chronic exposure to high blood glucose levels can lead to beta cell dysfunction and impaired insulin secretion, a phenomenon known as glucotoxicity. Glucotoxicity also contributes to a progressive decline in beta cell function, worsening hyperglycaemia over time. Metabolic syndrome describes a cluster of increased metabolic risk factors, including obesity, insulin resistance, dyslipidaemia, and hypertension. Individuals with metabolic syndrome are at increased risk of developing type 2 diabetes and cardiovascular disease. Lifestyle modifications, such as weight loss, increased physical activity, and dietary changes, are important strategies for managing metabolic syndrome and reducing diabetes risk.Finally, the management of diabetes involves interventions aimed at restoring metabolic balance and glycaemic control. For type 1 diabetes, insulin therapy is essential., whilst in type 2 diabetes, lifestyle modifications, oral medications, and/or injectable therapies, including insulin, are used to improve insulin sensitivity, reduce insulin resistance, and maintain blood glucose levels within normal target ranges. We provide a comprehensive product catalogue of research reagents for studying diabetes, including IRS1 antibodies, RBP4 antibodies, PTEN antibodies, BDNF ELISA Kits, and Adiponectin ELISA Kits. Explore our full diabetes product range below and discover more, for less.