No abstract

Glucose-dependent insulinotropic polypeptide (GIP) beyond its insulinotropic effects may regulate postprandial lipid metabolism. Whereas the insulinotropic action of GIP is known to be impaired in type 2 diabetes mellitus (T2DM), its adipogenic effect is unknown. We hypothesized that GIP is anabolic in human subcutaneous adipose tissue (SAT) promoting triacylglycerol (TAG) deposition through reesterification of nonesterified fatty acids (NEFA), and this effect may differ according to obesity status or glucose tolerance. Twenty-three subjects categorized into four groups, normoglycemic lean ( = 6), normoglycemic obese ( = 6), obese with impaired glucose regulation (IGR; = 6), and obese T2DM ( = 5), participated in a double-blind, randomized, crossover study involving a hyperglycemic clamp with a 240-min GIP infusion (2 pmol·kg·min) or normal saline. Insulin, NEFA, SAT-TAG content, and gene expression of key lipogenic enzymes were determined before and immediately after GIP/saline infusions. GIP lowered NEFA concentrations in the obese T2DM group despite diminished insulinotropic activity (mean NEFA AUC ± SE, 41,992 ± 9,843 µmol·l·min vs. 71,468 ± 13,605 with placebo, = 0.039, 95% CI: 0.31-0.95). Additionally, GIP increased SAT-TAG in obese T2DM (1.78 ± 0.4 vs 0.86 ± 0.1-fold with placebo, = 0.043, 95% CI: 0.1-1.8). Such effect with GIP was not observed in other three groups despite greater insulinotropic activity. Reduction in NEFA concentration with GIP correlated with adipose tissue insulin resistance for all subjects (Pearson, = 0.56, = 0.005). There were no significant gene expression changes in key SAT lipid metabolism enzymes. In conclusion, GIP appears to promote fat accretion and thus may exacerbate obesity and insulin resistance in T2DM.

There are approximately 2.5 million people in the UK with diabetes; 85-95% of whom have type 2 diabetes. Type 2 diabetes mellitus is characterized by insulin resistance and impaired insulin secretion. As approximately 90% of people with type 2 diabetes are overweight or obese, obesity is seen as a significant contributory factor in its development. This article aims to examine some of the physiological mechanisms by which overweight and obesity contribute to the development of type 2 diabetes, and review some of the approaches to managing overweight and obesity in the person with established type 2 diabetes, including dietary management, the use of reduced carbohydrate diets on glycamic control, anti-diabetes and anti-obesity drugs both in use and in development, and bariatric surgery.

Genetic variants in inflammation-related genes, specifically purinergic receptor P2X7, may be involved in susceptibility to childhood-onset febrile seizures.

Glucose monitoring is done to obtain information on blood glucose levels to ensure a therapeutic regimen; the aim is to maintain consistent glucose levels and avoid hypoglycaemia and hyperglycaemia. Self-management is central to diabetes control. Diabetes is individual, so self-monitoring of blood glucose (SMBG) targets and frequency of testing must be decided to meet each patient's needs. Nurses have key roles in education and advocacy. They can educate patients on what affects glucose levels, why they need to carry out SMBG, and how to interpret and act on the results. Nurses also match glucose monitoring meters to patients' needs by considering ease of use, technical features and lifestyle. Access to testing supplies is sometimes restricted through blanket policies and nurses have an advocacy role here in challenging inappropriate restrictions.