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A new type of immune system cell now comes to light in mice: the interferon-producing killer dendritic cell (IKDC). This cell shares many features with dendritic cells and with natural killer cells. It has cytotoxic and antitumor activity, produces interferons and develops antigen presentation capacity (pages 207–213 and 214–219).
Vascular endothelial cells respond to alarm signals of the body by angiogenesis or inflammation. The balance between these two responses is now pinned to two regulators of angiogenesis. Angiopoietin-1 dampens the inflammatory response, and angiopoietin-2 boosts it (pages 235–239).
Real-time imaging of malaria sporozoites in mammalian skin and lymph nodes gives new insight into parasite migratory behavior and transit through vasculature (pages 220–224).
Melanoma may be promoted by low oxygen conditions in the skin, which turn on the oxygen-response regulator HIF-1. HIF-1 seems to act in concert with well-established oncoproteins to promote tumorigenesis—a process that responds to the drug rapamycin.
Liver glucose production is crucial to survival during fast and is abnormally elevated in diabetes. Studies of the transcriptional coactivator Torc2 redefine the mechanism by which cAMP signaling affects fasting-induced glucogenesis.
Obesity-related chronic inflammation underlies insulin resistance, a key feature of type 2 diabetes. Recent data link the stress pathway of the endoplasmic reticulum to this phenomenon.
Comparing gene expression patterns of pancreatic islets from normal and diabetic people show that the transcription factor ARNT/HIF1β is the most markedly reduced in humans with the disease. ARNT regulates many beta-cell genes, insulin secretion and glucose tolerance.
Primary alterations in insulin signaling pathways are not the only way to reduce the body's sensitivity to insulin. By promoting the release of cytokines, liver inflammation can also lead to insulin resistance.
A spate of recent studies has identified key neural pathways that control glucose production from the liver. They may provide a new link between obesity and type 2 diabetes.
A cancer genetics dogma states that hematologic malignancies arise as a result of defined chromosomal translocations, whereas mutations underlie epithelial solid tumors. This rule is now broken in an analysis of chromosomal translocations in prostate cancer.
Changes in blood flow and hypoxia lead to endothelial-mediated control of vascular tone. An additional nucleotide receptor on endothelial cells has been identified that mediates release of nitric oxide and vasodilation (pages 133–137).
Defects in the ability of fat cells to transport glucose are linked to insulin resistance in muscle and liver. Retinol binding protein 4 (RBP4) now comes to the fore as a new adipokine, linking glucose uptake in adipocytes with systemic insulin sensitivity.
The interplay of factors that impair insulin signaling to cause type 2 diabetes is unclear, but one idea is that visceral fat might produce them. Visfatin, a protein previously known for its effect on immune cells, may be one of these factors.
Sirt1, an enzyme that removes acetyl groups from specific nuclear proteins, has been linked to the regulation of aging. It is now clear that Sirt1 also controls hepatic glucose metabolism by serving as a sensor of the metabolic status in hepatocytes.
Insulin secretion regulates glucose homeostasis and its dysregulation causes type 2 diabetes. Short noncoding microRNAs have now been shown to control exocytosis, the final event in insulin secretion. This discovery opens potential perspectives for diabetes therapy.
The transcriptional network downstream of the insulin receptor is incompletely understood, but recent data identify a new player. Foxa2—a forkhead transcription factor—controls hepatic lipid metabolism in fasting and type 2 diabetes, improving insulin resistance in peripheral tissues.
A reduction in mitochondrial activity and the subsequent decrease in energy expenditure contribute substantially to metabolic dysfunction in aging, insulin resistance and diabetes. Enhancing mitochondrial activity could improve metabolic homeostasis.
'Survival of the fittest' is based in part on the notion that genetic selection allows individuals to escape predators in the wild. A recent study indicates that selection for increased aerobic capacity may afford protection from cardiovascular risk factors associated with the metabolic syndrome.
