Quantitative physical variations in ripening of honey of indigenous hive bee apis cerana indica.

Physical factors of refractive index, optical density, viscosity and surface tension demonstrated quantitative change throughout five stages of honey ripening process in indigenous hive honeybee Apis cerana indica. The five stages of nectar to honey transformations include floral nectar (fn), honey crop of foragers (hf), honey crop of house bees (hh), unsealed honey cells (uh) and sealed honey cells (sh). All the four physical factors gradually augmented through successive stages of honey ripening phenomena. The refractive index of floral nectaries and sealed honey cells was 1.23 and 1.49 respectively. Similarly, the optical density of house bees and unsealed honey cells was 0.39 and 0.54 respectively. Viscosity and surface tension of honey crop of foragers and sealed honey cells were 0.15 poise, 0.76 dynes/cms. and 76.65 poise, 102.01 dynes/cms. respectively. The analysis of variance (ANOVA) of viscosity and surface tension in honey formation was significant at P<0.01% levels and refractive index and optical density of honey in ripening process was not significant at P<0.01% levels.

Quantitative chemical variations in ripening of honey of indigenous hive bee apis cerana indica.

Chemical characteristics of TRS, NRS, ash, acidity and pH were detected in five stages of honey ripening process of indigenous hive honeybee Apis cerana indica. Five stages of nectar to honey transformation comprise floral nectar (fn), honey crop of foragers (hf), honey crop of house bees (hh), unsealed honey cells (uh) and sealed honey cells (sh). The TRS of fn and sh cells was 2.12% and 73.01% respectively. Correspondingly NRS of hh and uh cells was 14.90% and 7.50%. The ash content of hf and sh cells was 0.20% and 1.49% respectively, whereas the acidity of sh cells and hf was 0.503 and 0.06 respectively. Similarly pH of hh and uh cells had a value of 1.03 and 2.61. All the five parameters viz., TRS, NRS, ash, acidity and pH tested apart from NRS were less in floral nectaries and maximum in sealed honey cells. The analysis of variance (ANOVA) of TRS of ripening of honey was significant at P<0.01% levels, while NRS, ash, acidity and pH in honey formation was not significant at P<0.01% levels.

Association of leukocyte count and hsCRP with metabolic abnormalities in subjects with normal glucose tolerance (CURES – 64).

Objective : The aim of the present study was to assess the association of leukocyte count and high sensitivity C-Reactive protein (hsCRP) with metabolic abnormalities in subjects with normal glucose tolerance. Methods : Subjects with Normal Glucose Tolerance (NGT) (n = 865) were recruited from the Chennai Urban Rural Epidemiology Study [CURES]. Standard methods were used for assessing hsCRP [Nephelometry, in a subset] and leukocytes [Flowcytometry, Sysmex SF-3000]. Insulin resistance was calculated using the Homeostasis Assessment model (HOMA-IR). Results : Body mass index, waist circumference, systolic and diastolic blood pressure, fasting plasma glucose, HbA1c, serum cholesterol, LDL cholesterol, HOMA IR and hsCRP increased significantly with increasing tertiles of leukocyte count [p for trend < 0.001]. Both leukocyte count and hsCRP showed a positive correlation with cardiovascular risk factors. Leukocyte count showed a positive correlation with hsCRP [p=0.008]. Both mean leukocyte count [p<0.001] and hsCRP [p=0.04] were higher in subjects with Metabolic Syndrome (MS), which increased with increase in number of metabolic abnormalities [p for trend <0.001]. Regression models showed leukocyte count [p<0.001] and hsCRP [p=0.03] to be associated with MS, even after adjusting for age and gender. Conclusion : A significant association exists between systemic inflammation [leukocyte count and hsCRP] and MS/ cardiovascular risk factors in Asian Indians even among non-diabetic subjects. ©

Telomere shortening & metabolic/vascular diseases.

Telomeres are specialized DNA-protein structures located at the ends of eukaryotic chromosomes whose length is progressively reduced in most somatic cells during ageing. Over the past decade, emerging evidence has shown that the telomeres are essential regulators of cellular life span and chromosome integrity in a dynamic fashion. By inducing genomic instability, replicative senescence and apoptosis, shortening of telomeres is thought to contribute to organismal ageing. While the aetiology of cardiovascular diseases and diabetes represent a complex interaction between various risk factors overlaid on different genetic backgrounds, the conventional risk factors often did not explain the inter-individual variability related to predisposition of disease states. This underscores the need for biological indicators of ageing in evaluating the aetiology of several age-related disorders, and recent studies indicate that telomere length could qualify as an ideal marker of biological ageing. Short telomeres have been detected in senescent endothelial cells and vascular smooth muscle cells from human atherosclerotic plaque as well as in myocardial tissue from patients with end-stage heart failure and cardiac hypertrophy. In addition, telomere shortening has been demonstrated in WBCs from patients with coronary heart disease, premature myocardial infarction, hypertension and diabetes mellitus. In this review, we discuss the telomere hypothesis of ageing as well as human studies that address the role of telomeres in cardiovascular, diabetes and other cardio-metabolic pathologies.

Endoplasmic reticulum (ER) stress & diabetes.

The endoplasmic reticulum (ER) is a central organelle entrusted with lipid synthesis, protein folding and protein maturation. It is endowed with a quality control system that facilitates the recognition and targeting of aberrant proteins for degradation. When the capacity of this quality control system is exceeded, a stress response (ER stress) is switched on. Prolonged stress leads to apoptosis and may thus be an important factor in the pathogenesis of many diseases. A complex homeostatic signaling pathway, known as the unfolded protein response (UPR), has evolved to maintain a balance between the load of newly synthesized proteins and the capacity of the ER to aid in their maturation. Dysfunction of the UPR plays an important role in certain diseases, especially those involving tissues dedicated to extracellular protein synthesis. Diabetes is an example of such a disease, since pancreatic beta-cells depend on efficient UPR signaling to meet the demands for constantly varying levels of insulin synthesis. Recent studies have indicated that the importance of the UPR in diabetes is not restricted to the beta-cell but also to tissues of peripheral insulin resistance such as liver and adipose tissue. Better understanding of the basic mechanisms of ER stress and development of insulin resistance/type 2 diabetes is pivotal for the identification of newer molecular targets for therapeutic interventions.

Curcumin-induced inhibition of cellular reactive oxygen species generation: novel therapeutic implications.

There is evidence for increased levels of circulating reactive oxygen species (ROS) in diabetics, as indirectly inferred by the findings of increased lipid peroxidation and decreased antioxidant status. Direct measurements of intracellular generation of ROS using fluorescent dyes also demonstrate an association of oxidative stress with diabetes. Although phenolic compounds attenuate oxidative stress-related tissue damage, there are concerns over toxicity of synthetic phenolic antioxidants and this has considerably stimulated interest in investigating the role of natural phenolics in medicinal applications. Curcumin (the primary active principle in turmeric, Curcuma longa Linn.) has been claimed to represent a potential antioxidant and antiinflammatory agent with phytonutrient and bioprotective properties. However there are lack of molecular studies to demonstrate its cellular action and potential molecular targets. In this study the antioxidant effect of curcumin as a function of changes in cellular ROS generation was tested. Our results clearly demonstrate that curcumin abolished both phorbol-12 myristate-13 acetate (PMA) and thapsigargin-induced ROS generation in cells from control and diabetic subjects. The pattern of these ROS inhibitory effects as a function of dose-dependency suggests that curcumin mechanistically interferes with protein kinase C (PKC) and calcium regulation. Simultaneous measurements of ROS and Ca2+ influx suggest that a rise in cytosolic Ca2+ may be a trigger for increased ROS generation. We suggest that the antioxidant and antiangeogenic actions of curcumin, as a mechanism of inhibition of Ca2+ entry and PKC activity, should be further exploited to develop suitable and novel drugs for the treatment of diabetic retinopathy and other diabetic complications.

Orally active insulin mimics: where do we stand now?

The war against diabetes through the development of new drugs is an ongoing continuous process to counter the alarming global increase in the prevalence of diabetes and its complications, particularly in developing countries like India. Unfortunately, the speed with which our knowledge of diabetes and its effects is expanding is not matched by the availability of new drugs. Following the identification of the insulin receptor (IR), its intrinsic kinase activity and molecular cloning, many studies have looked at IR as an ideal drug target. This review summarizes in brief the latest advancements in this field with particular reference to the current situation in respect of the development of orally active insulin mimetics in the treatment of type 2 diabetes.