CD36 expression and lipid metabolism following an oral glucose challenge in South Asians

AIM:To investigate lipid metabolism and the relationship with monocyte expression of the fatty acid translocase CD36 in South Asians.METHODS:An observational study of South Asians whom as an ethnic group have-a higher risk of developing diabetes.The susceptibility to diabetes is coupled with an earlier and more rapid progression of micro-,and macro-vascular complications.Twentynine healthy South Asian participants [mean age 34.6(8.9) years,76.2% male,mean body-mass index 25.0(5.2) kg/m2] were recruited from an urban residential area of central Birmingham(United Kingdom).The main outcomes measured were post prandial(30 min) and post absorptive(120 min) changes from fasting(0 min) in circulating lipoproteins,lipds and hormones,andmonocyte expression of CD36 post injection of a 75 g oral glucose challenge.The inducements of variations of monocyte CD36 expression were analysed.RESULTS:Our results showed evident changes in monocyte CD36 expression following the glucose challenge(P < 0.001).Non-esterified fatty acids(NEFA) levels decreased progressively during the challenge(P < 0.001),in contrast to increased cholesterol(but not triglyceride) concentrations within very low density lipoprotein(VLDL) and low density lipoprotein subfractions(P < 0.01).Levels of,glucose,serum triglycerides and high density lipoprotein cholesterol remained largely unchanged.Variations of monocyte CD36 were negatively(r =-0.47,P = 0.04) associated to fat from the diet and positively to carbohydrate from the diet(r = 0.65,P < 0.001).CONCLUSION:These data suggest that the initiation of VLDL genesis follows the consumption of glucose within this population,inferring that the sequestration of NEFA from these particles happens due to the increased availability of CD36 receptors.While these are preliminary results,it would appear that lifestyle exposures have a role in moderating the expression of CD36.

Tipping the balance:Haemoglobinopathies and the risk ofdiabetes

AIM: To establish a link between the risk of diabetes with haemoglobinopathies by examining available evidence of the effects of iron and blood glucose homeostasis from molecular to epidemiological perspectives.METHODS: A systematic literature search was performed using electronic literature databases using various search terms. The International Diabetes Federation World Atlas was used to generate a list of populations with high rates of diabetes. Pub Med, Scopus and Google Scholar were used to identify which of these populations also had a reported prevalence of haemoglobin abnormalities.RESULTS: Abnormalities in iron homeostasis leads to increases in reactive oxygen species in the blood. This promotes oxidative stress which contributes to peripheral resistance to insulin in two ways:(1) reduced insulin/insulin receptor interaction; and(2) β-cell dysfunction. Hepcidin is crucial in terms of maintaining appropriate amounts of iron in the body and is in turn affected by haemoglobinopathies. Hepcidin also has other metabolic effects in places such as the liver but so far the extent of these is not well understood. It does however directly control the levels of serum ferritin. High serum ferritin is found in obese patients and those with diabetes and a meta-analysis of the various studies shows that high serum ferritin does indeed increase diabetes risk.CONCLUSION: From an epidemiological standpoint, it is plausible that the well-documented protective effects of haemoglobinopathies with regard to malaria may have also offered other evolutionary advantages. By contributing to peripheral insulin resistance, haemoglobinopathies may have helped to sculpt the so-called "thrifty genotype", which hypothetically is advantageous in times of famine. The prevalence data however is not extensive enough to provide concrete associations between diabetes and haemoglobinopathies- more precise studies are required.