Area-level socioeconomic status and incidence of abnormal glucose metabolism : the Australian diabetes, obesity and lifestyle (AusDiab) study

OBJECTIVE--To examine the role of area-level socioeconomic status (SES) on the development of abnormal glucose metabolism (AGM) using national, population-based data.

RESEARCH DESIGN AND METHODS--The Australian Diabetes, Obesity and Lifestyle (AusDiab) study is a national, population-based, longitudinal study of adults aged [greater than or equal to] 25 years. A sample of 4,572 people provided complete baseline (1999 to 2000) and 5-year follow-up (2004 to 2005) data relevant for these analyses. Incident AGM was assessed using fasting plasma glucose and 2-h plasma glucose from oral glucose tolerance tests, and demographic, socioeconomic, and behavioral data were collected by interview and questionnaire. Area SES was defined using the Index of Relative Socioeconomic Disadvantage. Generalized linear mixed models were used to examine the relationship between area SES and incident AGM, with adjustment for covariates and correction for cluster design effects.

RESULTS--Area SES predicted the development of AGM, after adjustment for age, sex, and individual SES. People living in areas with the most disadvantage were significantly more likely to develop AGM, compared with those living in the least deprived areas (odds ratio 1.53; 95% CI 1.07-2.18). Health behaviors (in particular, physical activity) and central adiposity appeared to partially mediate this relationship.

CONCLUSIONS--Our findings suggest that characteristics of the physical, social, and economic aspects of local areas influence diabetes risk. Future research should focus on identifying the aspects of local environment that are associated with diabetes risk and how they might be modified.

Methazolamide is a new hepatic insulin sensitizer that lowers blood glucose in vivo

We previously used Gene Expression Signature technology to identify methazolamide (MTZ) and related compounds with insulin sensitizing activity in vitro. The effects of these compounds were investigated in diabetic db/db mice, insulin-resistant diet-induced obese (DIO) mice, and rats with streptozotocin (STZ)-induced diabetes. MTZ reduced fasting blood glucose and HbA1c levels in db/db mice, improved glucose tolerance in DIO mice, and enhanced the glucose-lowering effects of exogenous insulin administration in rats with STZ-induced diabetes. Hyperinsulinemic-euglycemic clamps in DIO mice revealed that MTZ increased glucose infusion rate and suppressed endogenous glucose production. Whole-body or cellular oxygen consumption rate was not altered, suggesting MTZ may inhibit glucose production by different mechanism(s) to metformin. In support of this, MTZ enhanced the glucose-lowering effects of metformin in db/db mice. MTZ is known to be a carbonic anhydrase inhibitor (CAI); however, CAIs acetazolamide, ethoxyzolamide, dichlorphenamide, chlorthalidone, and furosemide were not effective in vivo. Our results demonstrate that MTZ acts as an insulin sensitizer that suppresses hepatic glucose production in vivo. The antidiabetic effect of MTZ does not appear to be a function of its known activity as a CAI. The additive glucose-lowering effect of MTZ together with metformin highlights the potential utility for the management of type 2 diabetes.

Subjective wellbeing homeostasis

This chapter explains the concept of subjective well-being homeostasis. It concerns the proposal that subjective well-being (SWB) is managed by a system of psychological devices which have evolved for this purpose. The chapter begins by presenting some of the psychometric characteristics of SWB and introduces homeostasis as a theoretical construct that can account for these characteristics. This is followed by a discussion of the relationship between SWB and depression. The chapter ends with recommendations for measurement scales.

High glucose-induced impairment in insulin secretion is associated with reduction in islet glucokinase in a mouse model of susceptibility to islet dysfunction

Type 2 diabetes is characterized by islet dysfunction resulting in hyperglycemia, which can then lead to further deterioration in islet function. A possible mechanism for hyperglycemia-induced islet dysfunction is the accumulation of advanced glycation end products (AGE). The DBA/2 mouse develops pancreatic islet dysfunction when exposed to a high glucose environment and/or obesity-induced insulin resistance. To determine the biochemical cause of dysfunction, DBA/2 and C57BL/6 control islets were incubated in 11.1 mM or 40 mM glucose in the absence or presence of the AGE inhibitor aminoguanidine (AG) for 10 days. Basal (2.8 mM glucose) insulin release was increased in both DBA/2 and C57BL/6 islets incubated with 40 mM vs 11.1 mM glucose for 10 days. Chronic exposure to hyperglycemia decreased glucose (20 mM)-stimulated insulin secretion in DBA/2 but not in C57BL/6 islets. AG significantly increased fold-induced insulin release in high glucose cultured DBA/2 mouse islets, but did not affect C57BL/6 islet function. DBA/2 islet glucokinase was significantly reduced following 40 mM glucose culture, compared with 11.1 mM glucose cultured DBA/2 islets and 40 mM glucose cultured C57BL/6 islets. Incubation of islets with AG resulted in a normalization of DBA/2 islet glucokinase levels. In conclusion, chronic high glucose-induced increases in AGE can result in islet dysfunction and this is associated with reduced glucokinase levels in a mouse model with susceptibility to islet failure.

Lack of glucose and hsp70 responses in haddock Melanogrammus aeglefinus (L.) subjected to handling and heat shock

Juvenile haddock Melanogrammus aeglefinus (c. 39 g) were exposed to either a handling stressor (1 min out of water) or heat shock (increase from 10 to 15° C for 1 h), and plasma cortisol, plasma glucose and gill hsp70 levels were determined before, and at 1, 3, 6, 12, 24 and 48 h post-stress. The pattern of cortisol increase was similar following both stressors, with levels increasing by 25-fold at 1 h post-stress, but returning to pre-stress levels (2–5 ng ml⁻¹) by 3 h. In contrast, neither handling nor heat shock caused an increase in plasma glucose levels. Although gill hsp70 was detected, presumably constitutive levels, in both control and heat shocked groups, there were not significant changes in gill hsp70 levels after exposure to heat shock. The lack of glucose and hsp70 responses to these typical stressors is consistent with previous studies on Atlantic cod Gadus morhua, and suggests that the stress physiology of Gadidae differs from the ‘typical’ teleost.

A novel non-enzymatic glucose sensor based on nickel (II) oxide electrospun nanofibers

A new enzymeless glucose sensor has been fabricated via electrospinning technology and subsequent calcination. The morphology and structure of the as-prepared nanofibers have been characterized by scanning electron microscopy (SEM), transmission electron microscopy (TEM), and X-ray diffraction (XRD). The electrocatalytic oxidation of glucose in alkaline medium at nickel oxide modified glassy carbon electrodes has been investigated. The modified electrodes offer excellent electrocatalytic activity toward the glucose oxidation at low positive potential (0.3 V). Glucose has been determined chronoamperometrically at the surface of NiO nanofibers modified electrode in 0.5 mM NaOH. Under the optimized condition, the calibration curve is linear in the concentration range of 2 × 10−3 mM∼1 mM, and 1 mM∼9.5 mM. The detection limit (signal-to-noise 3) and response time are 3.394 × 10−6 M and 2 s, respectively. The NiO electrospun nanofibers is easy to prepare and feasible in economy. The modified electrode is steady and can be used repeatedly, so it is reasonable to expect its broad use in non-enzymatic glucose sensor.

Consumption of a low glycaemic index diet in late life extends lifespan of Balb/c mice with differential effects on DNA damage

Background : Caloric restriction is known to extend the lifespan of all organisms in which it has been tested. Consequently, current research is investigating the role of various foods to improve health and lifespan. The role of various diets has received less attention however, and in some cases may have more capacity to improve health and longevity than specific foods alone. We examined the benefits to longevity of a low glycaemic index (GI) diet in aged Balb/c mice and examined markers of oxidative stress and subsequent effects on telomere dynamics.

Results : In an aged population of mice, a low GI diet extended average lifespan by 12%, improved glucose tolerance and had impressive effects on amelioration of oxidative damage to DNA in white blood cells. Telomere length in quadriceps muscle showed no improvement in the dieted group, nor was telomerase reactivated.

Conclusion : The beneficial effects of a low GI diet are evident from the current study and although the impact to telomere dynamics late in life is minimal, we expect that earlier intervention with a low GI diet would provide significant improvement in health and longevity with associated effects to telomere homeostasis.