ABSTRACT
Diabetes mellitus [DM] is a global health problem with high morbidity and mortality. The prevalence of DM is on the increase in many parts of the world, especially in the Gulf region. Many studies from this region have reported different prevalence rates for the six Gulf Cooperation Council countries. Prevalence is estimated at between 9% and 25% in Bahrain, 16.1% in Oman, 21.4% in Kuwait, 16.7% in Qatar, 23.7% in Saudi Arabia and 23.3% in the United Arab Emirates. These reports show that the prevalence of DM is high in Gulf Cooperation Council countries compared with other regions of the world, except for the Pacific islands. A concerted effort is needed to combat the increasing prevalence of DM
ABSTRACT
Diabetes mellitus and its complications is a serious global health problem and the total number of people with this disease is projected to rise from 171 million in 2000 to 366 million in 2030. A recent study among Emirati citizens reported age-standardized rates for diabetes mellitus [diagnosed and undiagnosed] and pre-diabetes in those 30-64 years old as 29.0% and 24.2%, respectively. The association between type 2 diabetes mellitus and obesity is very strong and cardiovascular disease is the leading cause of morbidity and mortality among diabetic patients. The changes in ventricular myocyte contraction, intracellular calcium and the expression of genes encoding cardiac muscle proteins that take place in young [9-13 weeks] and ageing [30-34 weeks] Zucker diabetic fatty [ZDF] rat heart have been reviewed. Diabetes mellitus was associated with a fourfold elevation in non-fasting blood glucose in young and ageing ZDF rat compared with age-matched Zucker lean controls. Amplitude of shortening was unaltered in myocytes from young and ageing ZDF rats. Time to peak and time to half relaxation of shortening was prolonged in myocytes from young ZDF rats and was unaltered in myocytes from ageing ZDF rats compared with controls. Amplitude of the Ca[2+] transient was unaltered in myocytes from young and ageing ZDF rats. Time to peak Ca[2+] transient was prolonged in myocytes from young and ageing ZDF rats. L-type Ca[2+] current was significantly reduced in myocytes from young and ageing ZDF rats. Sarcoplasmic reticulum Ca[2+] transport did not appear to be altered in myocytes from young or ageing ZDF rats. Expression of genes encoding L-type Ca[2+] channel proteins, plasma membrane transporters, sarcoplasmic reticulum Ca[2+] and regulatory proteins and cardiac muscle proteins were variously up-regulated, down-regulated or unaltered in ventricles from young and ageing ZDF rats. Up-regulated genes in young ZDF rat heart included CACNA[1C], CACNA1G, CACNA1H, ATP1A1 and MYH7, whereas down-regulated genes in young ZDF rat heart included ATP1B1, SLC9A1, ATP2A2, CALM1, MYH6, MYL2, ACTC1, TNNI3, TNNT2 and TNNC1. Up-regulated genes in ageing ZDF rat heart included CACNA1G, CACNA1H, ATP2A1 and MYL2, whereas down-regulated genes in ageing ZDF rat heart included CACNA2D3, SLC9A1, ATP2A2, MYH6 and TNNT2. Subtle changes in expression of genes encoding various cardiac muscle proteins may underlie functional changes in hearts of young and ageing ZDF rats compared with age-matched controls
ABSTRACT
Diabetes mellitus [DM] is a major global health problem and it currently affects more than 175 million people worldwide. DM is an increasingly common chronic disorder which is associated with substantial costs in terms of life and demand on health budgets. Thus, up to 15% of national budgets are spent on the diagnosis, treatment and caring of diabetic patients in the Western World. DM is divided into two main groups, Type 1 or Insulin -dependent diabetes mellitus [IDDM; 5-10 % of all cases and juvenile onset] and Type 2 or Non-insulin- dependent diabetes mellitus [NIDDM; 90-95 % of all cases and adult in onset]. Both Types 1 and 2 DM are associated with a number of common symptoms and long term complications. One of these is the indigestion of food stuffs, especially carbohydrates. This is due to the inability of the gastrointestinal tract, especially the salivary glands and the exocrine pancreas to secrete an adequate amount of the major digestive enzyme, amylase. The medical term used to describe the dysfunction is digestive insufficiency or exocrine pancreatic insufficiency when dealing with the pancreas alone. Current evidence in the literature suggests that exocrine pancreatic insufficiency may be associated with a number of physiological and biochemical processes which may be deranged in the pancreas. These include reduced endogenous insulin secretion or insensitivity of the islet hormone to regulate glucose metabolism especially by pancreatic acinar cells, reduced gene expression for the mRNA amylase and the synthesis and release of the enzyme, reduced cytosolic concentrations of calcium [ca2+] and magnesium [Mg2] Na+ - k+ -ATP pase and tyrosine kinase activities and insensitivity of cholecystokinin [CCK] receptors on pancreatic acinar cells. This review describes the cellular mechanism of exocrine pancreatic insufficiency in DM compared to healthy conditions. The work focuses on a brief review of DM, the normal anatomy and physiology of the pancreas, stimulus-secretion coupling and the interactions between secretagogues, DM-induced exocrine pancreatic insufficiency and the roles of a number of cellular mediators in the stimulus- secretion coupling processes, the cellular and molecular mechanisms associated with the disease and finally, on the scope for future research studies