Diabetologia

Edlund, H.

doi: 10.1007/s001250100623pmid: 11596660

Diabetes affects 4 to 5 % of the population worldwide and is the most common metabolic disorder. The number of individuals diagnosed with diabetes is rapidly increasing, especially in the developed countries and the disorder frequently leads to secondary complications such as retinopathy, nephropathy, neuropathy and cardiovascular disease. Type II (non-insulin-dependent) diabetes mellitus is the most common form of diabetes, more than 90 % of diagnosed cases, and results from insulin resistance, pancreatic beta-cell dysfunction, or a combination of both. The beta-cell dysfunction seems to result in part from an inability of the beta cells to produce and secrete sufficient amounts of active insulin in response to an increased demand for insulin. Type I (insulin-dependent) diabetes mellitus is caused by an autoimmune destruction of the insulin producing beta cells, resulting in insulin deficiency. The existing therapies for both types of diabetes are unsatisfactory since they do not offer a cure and are mostly not sufficient for preventing the secondary complications associated with diabetes. Thus, there is a great need for new improved therapies. This search is, however, hampered by our currently limited knowledge of the basic processes that control the proliferation, differentiation, survival and physiology of the beta cell. Over the last 7 to 8 years our knowledge concerning the development of the pancreas has increased substantially due to the use of genetically modified mice. Nevertheless, key questions regarding the control of proliferation and differentiation of pancreatic progenitor cells into fully functional beta cells remain to be solved. (Diabetologia (2001) 44: 1071–1079)

Stacher, G.

doi: 10.1007/s001250100619pmid: 11596661

Many patients with diabetes mellitus complain of early satiety and postprandial gastric fullness. In 1945, these symptoms were first found to result from a gastric motor dysfunction which makes the delivery of ingesta into the small intestine, the time of their absorption and the related blood-glucose rise unpredictable. Consequently, insulin or hypoglycaemic agents are administered at inappropriate time points and poor glycaemic control ensues. About 50 % of patients with Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus are affected. Hyperglycaemia may play an important role in the disorder: gastric emptying was found to be slower in states of induced hyperglycaemia than in euglycaemia. However, significantly reduced blood-glucose concentrations after therapy readjustment were not associated with an increase in emptying rate. Prolonged hyperglycaemia could alter nerve metabolism and contribute to the development of neuropathy. Severity of cardiovascular autonomic neuropathy, but not actual blood-glucose and glycated haemoglobin level, has been found to correlate with the degree of emptying impairment. Drugs enhancing gastric emptying could improve the coordination between insulin administration and the onset of nutrient absorption and thus glycaemic control. Disappointingly, trials to study the long-term effects of such drugs are scarce and their results predominantly negative. In conclusion, many diabetic patients have impaired gastric motor function which could contribute to poor glycaemic control. Evidence suggests that autonomic neuropathy is the main underlying factor. This review aims to offer a critical survey of all the data available at present on these topics. (Diabetologia (2001) 44: 1080–1093)

Ramachandran, A.; Snehalatha, C.; Kapur, A.; Vijay, V.; Mohan, V.; Das, A. K.; Rao, P. V.; Yajnik, C. S.; Prasanna Kumar, K. M.; Nair, Jyotsna D.

doi: 10.1007/s001250100627pmid: 11596662

Obrosova, I. G.; Minchenko, A. G.; Marinescu, V.; Fathallah, L.; Kennedy, A.; Stockert, C. M.; Frank, R. N.; Stevens, M. J.

doi: 10.1007/s001250100631pmid: 11596663

Oxidative stress is directly involved in up regulation of vascular endothelial growth factor protein in the retina during early diabetes. (Diabetologia (2001) 44: 1102–1110)

Kaser, S.; Sandhofer, A.; Föger, B.; Ebenbichler, C. F.; Igelseder, B.; Malaimare, L.; Paulweber, B.; Patsch, J. R.

doi: 10.1007/s001250100630pmid: 11596664

This data suggests that increased phospholipid transfer protein activity in obese subjects is a consequence of obesity itself without the contribution of insulin resistance and can be explained by increased synthesis of phospholipid transfer protein from the enlarged mass of adipose tissue. (Diabetologia (2001) 44: 1111–1117)

ADVANCE Management Committee

doi: 10.1007/s001250100612pmid: 11596665

ADVANCE is designed to provide reliable evidence on the balance of benefits and risks conferred by blood pressure lowering therapy and intensive glucose control therapy in high-risk diabetic patients, regardless of initial blood pressure or glucose concentrations. (Diabetologia (2001) 44: 1118–1120)

Nordt, T. K.; Bode, C.; Sobel, B. E.

doi: 10.1007/s001250100618pmid: 11596666

Hyperproinsulinaemia can contribute to increased expression of plasminogen activator inhibitor type-1 in intra-abdominal adipose tissue implicated in increasing PAI-1 activity in blood, impaired fibrinolysis, and accelerated atherogenesis typical of Type II diabetes. (Diabetologia (2001) 44: 1121–1124)

Kellerer, M.; Lammers, R.; Fritsche, A.; Strack, V.; Machicao, F.; Borboni, P.; Ullrich, A.; Häring, H. U.

doi: 10.1007/s001250100614pmid: 11596667

In summary, our data suggest that the insulin receptor signalling pathway interferes with leptin signalling at the level of JAK-2. Inhibition of JAK-2 phosphorylation might occur through SHP-1-dependent pathways, indicating that hyperinsulinaemia contributes to the pathogenesis of leptin resistance. (Diabetologia (2001) 44: 1125–1132)

Osmond, D. T. D.; King, R. G.; Brennecke, S. P.; Gude, N. M.

doi: 10.1007/s001250100609pmid: 11596668

These results suggest that materno-fetal glucose transport increases in the placentae of women with gestational diabetes mellitus who receive insulin compared with those women who do not receive insulin. (Diabetologia (2001) 44: 1133–1139)

Karlsson, M. G. E.; Garcia, J.; Ludvigsson, J.

doi: 10.1007/s001250100611pmid: 11596669

Proteins from cows' milk caused an equal Th1- and Th2-like immune response in diabetic and healthy children. Thus, our results do not support the hypothesis that cows' milk antigens are important for the immune process associated with Type I diabetes. (Diabetologia (2001) 44: 1140–1147)