Diabetes and effect between little sleep

In 2005, a study of over 1400 participants showed that participants who habitually slept few hours were more likely to have associations with Diabetes Type 2. However, because this study was merely cor-relational, the direction of cause and effect between little sleep and diabetes is uncertain. The authors point to an earlier study which showed that experimental rather than habitual restriction of sleep resulted in impaired glucose tolerance (IGT).And  new mothers   sleep  pattern  are  also  very  poor. .
Researcher Dr Hawley E. Montgomery-Downs, said the study challenges a central assumption about new mothers' typical sleep patterns.
She said that the general assumption had been that most new mothers are not getting enough hours of sleep so the advice on how to combat daytime fatigue has focused on countering sleep deprivation, such as nap when your baby naps.For detail go to http://en.wikipedia.org

Diabetes ! Can lead to decrease in perlecan levels

Perlecan levels are decreased in many disease states - e.g., diabetes, atherosclerosis and arthritis. Perlecan has an important role in the maintenance of the glomerular filtration barrier. Decreased perlecan in the glomerular basement membrane has a central role in the development of diabetic albuminuria. Perlecan expression is down regulated by many atherogenic stimuli and thus Perlecan is thought to play a protective role in atherosclerosis. Diabetes and atherosclerosis are commonly associated syndromes. 80% of diabetes-associated deaths involve some form of atherosclerotic complication, and the basement membrane of endothelia has been implicated in the atherogenic process.Then  what  is Perlecan ?Heparan sulfate proteoglycan 2 (HSPG2), is a human gene which encodes the perlecan protein.
Perlecan is a large multidomain proteoglycan that binds to and cross-links many extracellular matrix (ECM) components and cell-surface molecules. Perlecan is synthesized by both vascular endothelial and smooth muscle cells and deposited in the extracellular matrix. Perlecan is highly conserved across species and the available data indicate that it has evolved from ancient ancestors by gene duplication and exon shuffling.

Synthesis of heparan sulfate was shown to decrease in the arteries of diabetics and in arteries developing atherosclerotic lesions. The mechanism by which heparan sulfate was downregulated in these lesions remained unknown for some time. One theory states that high glucose in circulation could lead to a decrease in GAG chain attachment to perlecan, but not necessarily a change in the synthetic pathway of the GAG chains or that of the core protein. After treatment of human aortic endothelial cells with high glucose medium, secreted perlecan contained less sulfate incorporation accompanied by less overall GAG chain incorporation. Although no signaling pathway is identified leading to this decrease in GAG chain incorporation, it is suggested that the 30% loss in overall glycosylation of the protein could mean loss of one of the three HS chains on perlecan in this model of diabetes-associated hyperglycemia. It is also noted that similar decreases in extracellular HS without a change in staining for the core protein chains occur in diabetic kidneys and in kidney cells in culture treated with high glucose.
SOURCE:http://en.wikipedia.org