Adherence to postpartum diabetes mellitus screening, do associated pregnancy complications make a difference?

AIMS: We aimed to investigate the impact of Gestational Diabetes Mellitus (GDM) complications on compliance with postpartum Diabetes screening. METHODS: A retrospective cohort study was conducted comparing screening rates of women with and without GDM associated complications who delivered at the Soroka University Medical Center, between 2016 and 2017. The screening test of choice was a 2-hour 75 g oral glucose tolerance test, taken 6-12 weeks after delivery. GDM associated complications included one or more of the following: polyhydramnios, macrosomia, shoulder dystocia or cesarean section. Univariate analysis was used in order to examine if GDM associated complications were associated with postpartum diabetes screening. RESULTS: During the study period a 164 women were included, of which, 82 women had suffered from GDM associated complications and comprised the study group and 82 women with GDM but without complications comprised the comparison group. Women in the study group were significantly older with a higher parity order. Induction rates were significantly higher among the comparison group, whereas, cesarean section rates were higher among the study group. No difference was noted with regard to neonatal outcomes. Women in the study group were not found to be more likely to be given screening recommendations at discharge (P = 0.50), at their postpartum visit (P = 0.36) or to perform DM screening postpartum (P = 0.17). CONCLUSION: Women with GDM associated complications had a higher rate of compliance to postpartum DM screening recommendations. However, in the current study this difference did not reach statistical significance.

Impaired Glucose Tolerance and Reduced Plasma Insulin Precede Decreased AKT Phosphorylation and GLUT3 Translocation in the Hippocampus of Old 3xTg-AD Mice.

Several studies have demonstrated that mouse models of Alzheimer's disease (AD) can exhibit impaired peripheral glucose tolerance. Further, in the APP/PS1 mouse model, this is observed prior to the appearance of AD-related neuropathology (e.g., amyloid-ß plaques; Aß) or cognitive impairment. In the current study, we examined whether impaired glucose tolerance also preceded AD-like changes in the triple transgenic model of AD (3xTg-AD). Glucose tolerance testing (GTT), insulin ELISAs, and insulin tolerance testing (ITT) were performed at ages prior to (1-3 months and 6-8 months old) and post-pathology (16-18 months old). Additionally, we examined for altered insulin signaling in the hippocampus. Western blots were used to evaluate the two-primary insulin signaling pathways: PI3K/AKT and MAPK/ERK. Since the PI3K/AKT pathway affects several downstream targets associated with metabolism (e.g., GSK3, glucose transporters), western blots were used to examine possible alterations in the expression, translocation, or activation of these targets. We found that 3xTg-AD mice display impaired glucose tolerance as early as 1 month of age, concomitant with a decrease in plasma insulin levels well prior to the detection of plaques (∼14 months old), aggregates of hyperphosphorylated tau (∼18 months old), and cognitive decline (≥18 months old). These alterations in peripheral metabolism were seen at all time points examined. In comparison, PI3K/AKT, but not MAPK/ERK, signaling was altered in the hippocampus only in 18-20-month-old 3xTg-AD mice, a time point at which there was a reduction in GLUT3 translocation to the plasma membrane. Taken together, our results provide further evidence that disruptions in energy metabolism may represent a foundational step in the development of AD.

Insulin resistance, weight, and behavioral variables as determinants of brain reactivity to food cues: a Prevention of Diabetes through Lifestyle Intervention and Population Studies in Europe and around the World - a PREVIEW study.

Background: Obesity and type 2 diabetes have been linked to alterations in food reward processing, which may be linked to insulin resistance. Objectives: In this clinical study, we investigated the respective contribution of insulin resistance, anthropometric measurements, and behavioral factors to brain reward activation in response to visual stimuli. Design: Food reward-related brain reward activation was assessed with functional magnetic resonance imaging in 39 overweight or obese individuals with impaired fasting glucose, impaired glucose tolerance, or both [22 women, 17 men; mean ± SD insulin sensitivity index (ISI): 2.7 ± 1.3; body mass index (BMI; kg/m2): 32.3 ± 3.7; body fat percentage: 40.5% ± 7.9%; fasting glucose: 6.3 ± 0.6 mmol/L]. Food and nonfood images were shown in a randomized block design. Brain activation (food compared with nonfood images) was correlated with anthropometric and behavioral variables. Behavioral variables included eating behavior [Three-Factor Eating Questionnaire (TFEQ)] and habitual physical activity (Baecke). Glucose and insulin concentrations, determined during an oral-glucose challenge, were used to assess the homeostatic model assessment for insulin resistance (HOMA-IR) and Matsuda ISI. Results: Food compared with nonfood brain activation was positively associated with HOMA-IR in the nucleus accumbens, right and left insula, and right cingulate gyrus (P < 0.005, corrected for multiple comparisons). TFEQ factor 2 was positively related to food compared with nonfood brain activation in the supramarginal gyrus (P < 0.005, corrected for multiple comparisons). Habitual physical activity during leisure time was negatively associated with food compared with nonfood brain activation in multiple regions associated with the attention and reward network (P < 0.005, corrected for multiple comparisons). Conclusions: Individuals with increased insulin resistance and emotional eating or disinhibition showed higher brain reactivity to food cues, which may imply changes in food preference and hyperphagia. Individuals with higher habitual physical activity showed less food reward-related brain activation.

Associations of Brain Reactivity to Food Cues with Weight Loss, Protein Intake and Dietary Restraint during the PREVIEW Intervention.

The objective was to assess the effects of a weight loss and subsequent weight maintenance period comprising two diets differing in protein intake, on brain reward reactivity to visual food cues. Brain reward reactivity was assessed with functional magnetic resonance imaging in 27 overweight/obese individuals with impaired fasting glucose and/or impaired glucose tolerance (HOMA-IR: 3.7 ± 1.7; BMI: 31.8 ± 3.2 kg/m²; fasting glucose: 6.4 ± 0.6 mmol/L) before and after an 8-week low energy diet followed by a 2-year weight maintenance period, with either high protein (HP) or medium protein (MP) dietary guidelines. Brain reactivity and possible relationships with protein intake, anthropometrics, insulin resistance and eating behaviour were assessed. Brain reactivity, BMI, HOMA-IR and protein intake did not change differently between the groups during the intervention. In the whole group, protein intake during weight maintenance was negatively related to changes in high calorie images>low calorie images (H > L) brain activation in the superior/middle frontal gyrus and the inferior temporal gyrus (p < 0.005, corrected for multiple comparisons). H > L brain activation was positively associated with changes in body weight and body-fat percentage and inversely associated with changes in dietary restraint in multiple reward, gustatory and processing regions (p < 0.005, corrected for multiple comparisons). In conclusion, changes in food reward-related brain activation were inversely associated with protein intake and dietary restraint during weight maintenance after weight loss and positively associated with changes in body weight and body-fat percentage.

Sexual functioning and depressive symptoms in men with various types of prediabetes: a pilot study.

No study has compared sexual functioning and depressive symptoms in male subjects with various types of prediabetes. Our study included four age- and weight-matched groups of apparently healthy men (25-50 years old): subjects with isolated impaired fasting glucose (IFG) (n = 16), men with isolated impaired glucose tolerance (n = 17), individuals with the presence of both IFG and impaired glucose tolerance (n = 16), as well as men with normal glucose tolerance (n = 18). All included men completed questionnaires evaluating male sexual functioning (IIEF-15) and assessing the presence and severity of depressive symptoms (BDI-II). Men with both IFG and impaired glucose tolerance obtained lower domain scores for erectile function, sexual desire, and overall satisfaction, as well as the higher overall BDI-II score. Individuals with isolated impaired glucose tolerance (IGT) and IFG were characterized by lower domain score only for sexual desire. In all study groups, domain score for erectile function correlated with the BDI-II score, while scores for erectile function and sexual desire correlated with a degree of insulin resistance. The obtained results suggest that prediabetes may impair sexual functioning in young men. The risk is particularly high in individuals with the presence of both IFG and IGT.

The relationship between sleep and cognitive function in patients with prediabetes and type 2 diabetes.

AIMS: Diabetes is linked to cognitive impairment. Sleep plays a role in memory consolidation. Sleep disturbances, commonly found in patients with diabetes, were shown to be related to cognitive dysfunction. This study explored the role of sleep in cognitive function of patients with abnormal glucose tolerance. METHODS: A total of 162 patients (81 type 2 diabetes and 81 prediabetes) participated. Sleep duration and sleep efficiency (an indicator of sleep quality) were obtained using 7-day actigraphy recordings. Obstructive sleep apnea (OSA) was screened using an overnight in-home monitor. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA). Three sub-scores of MoCA, visuoexecutive function, attention and delayed recall, were also analyzed. RESULTS: Mean age was 54.8 (10.2) years. OSA was diagnosed in 123 participants (76.9%). Mean sleep duration was 6.0 (1.0) h and sleep efficiency was 82.7 (8.1) %. Sleep duration and OSA severity were not related to MoCA scores. Higher sleep efficiency was associated with higher MoCA scores (p = 0.003), and having diabetes (vs. prediabetes) was associated with lower MoCA scores (p = 0.001). After adjusting covariates, both having diabetes (vs. prediabetes) (B = - 1.137, p = 0.002) and sleep efficiency (B = 0.085, p < 0.001) were independently associated with MoCA scores. In addition, diabetes (B = - 0.608, p < 0.001) and sleep efficiency (B = 0.038, p < 0.001) were associated with visuoexecutive function. Sleep parameters were not related to delayed recall or attention scores. CONCLUSION: Lower sleep efficiency is independently associated with lower cognitive function in patients with abnormal glucose tolerance. Whether sleep optimization may improve cognitive function in these patients should be explored.

Short-term thermoneutral housing alters glucose metabolism and markers of adipose tissue browning in response to a high-fat diet in lean mice.

Systemic insulin resistance and glucose intolerance occur with as little as 3 days of a high-fat diet (HFD) in mice and humans; the mechanisms that initiate acute insulin resistance are unknown. Most laboratories house mice at 22°C, which is below their thermoneutral temperature (~30°C). Cold stress has been shown to increase white adipose tissue (WAT) browning, alter lipid trafficking, and impair immune function, whereas energy intake and expenditure decrease with increasing ambient temperature; importantly, dysregulation of these parameters has been strongly linked to obesity-induced insulin resistance. Therefore, we compared acute changes in glucose metabolism and the metabolic phenotype in lean mice in response to a control diet or HFD housed at standard vivarium (22°C) and thermoneutral (30°C) temperatures. Glucose intolerance occurred following 1 or 5 days of HFD and was independent of housing temperature or adiposity; however, the reduction in tissue-specific glucose clearance with HFD diverged by temperature with reduced brown adipose tissue (BAT) glucose uptake at 22°C but reduced soleus glucose uptake at 30°C. Fasting glucose, food intake, and energy expenditure were significantly lower at 30°C, independent of diet. Additionally, markers of browning in both BAT and inguinal subcutaneous WAT, but not perigonadal epididymal WAT, decreased at 30°C. Together, we find housing temperature has a significant impact on the cellular pathways that regulate glucose tolerance in response to an acute HFD exposure. Thus, even short-term changes in housing temperature should be highly considered in interpretation of metabolic studies in mice.

Cardiovascular risk factors and glucose tolerance in midlife and risk of cognitive disorders in old age up to a 49-year follow-up of the Helsinki businessmen study.

PURPOSE: The purpose of this study is to compare midlife predictors of old age dementia with or without concomitant atherosclerotic cardiovascular disease (ASCVD). DESIGN: In the Helsinki Businessmen Study (men born in 1919-1934, n = 3309), death certificates (n = 1885) during up to 49-year follow-up (through 31 December 2013) were screened for dementia (n = 365) and ASCVD, and categorized as (1) AD without ASCVD ("pure" AD, n = 93), (2) AD + ASCVD (n = 126), (3) vascular dementia (VD, n = 82), (4) other or undefined etiology (n = 64). Using Cox analyses, death without dementia and dementia types were compared for the prediction by midlife ASCVD risk factors. Men without diagnosed dementia during follow-up were used as reference. RESULTS: ASCVD risk factors predicted death without dementia during follow-up. Midlife cholesterol was higher in AD + ASCVD and VD as compared with men surviving to old age without known dementia. None of the midlife factors including cholesterol and glucose tolerance predicted pure AD, but midlife cholesterol predicted AD + ASCVD, both as a continuous (hazard ratio [HR] per SD 1.24, 95% CI, 1.04-1.47), and dichotomous variable (cutpoint 6.5 mmol/L; HR 1.67, 95% CI, 1.16-2.40). CONCLUSION: Midlife cholesterol predicted dementia with vascular features, but midlife vascular risk factors and glucose intolerance were not related to pure Alzheimer disease without concomitant atherosclerotic cardiovascular disease. Key messages Heterogenous etiology of dementia, which in old age is usually a clinical diagnosis, may confound the role of long-term risk factors. In a longitudinal study with autopsy records, midlife cholesterol predicted dementia with features of atherosclerotic cardiovascular disease but not "pure" Alzheimer disease Glucose tolerance in midlife was not associated with pure Alzheimer's disease.

Low vitamin D levels are not a contributing factor to higher prevalence of depressive symptoms in people with Type 2 diabetes mellitus: the Hoorn study.

AIM: To test whether a low serum 25-hydroxyvitamin D level explains the greater prevalence of depression among people with Type 2 diabetes. METHODS: We performed a cross-sectional analysis of 527 people, aged 60-87 years, who participated in a population-based cohort study. Type 2 diabetes, impaired glucose tolerance, impaired fasting glucose and normal glucose tolerance were defined according to the 2006 WHO criteria. The Centre for Epidemiologic Studies Depression questionnaire was administered, using a cut-off score of ≥ 16 to determine clinically relevant depressive symptoms. RESULTS: Logistic regression analysis confirmed that women with impaired glucose tolerance/impaired fasting glucose and people with Type 2 diabetes did have a higher risk of depressive symptoms [unadjusted odds ratios 3.66 (95% CI 1.59 to 8.43) and 3.04 (95% CI 1.57 to 5.88), respectively], compared with people with normal glucose tolerance. Serum 25-hydroxyvitamin D level was not a mediating factor in the association between impaired glucose tolerance/impaired fasting glucose or Type 2 diabetes and depressive symptoms [unstandardized indirect effect 0.001 (95% CI -0.063 to 0.079) and 0.004 (95% CI -0.025 to 0.094), respectively]. CONCLUSIONS: The study found no evidence that low vitamin D levels are a contributing factor to higher depression scores in people with Type 2 diabetes.

Prevalence, awareness and risk factors of diabetes in Ahvaz (South West of Iran).

INTRODUCTION: This study was designed to assess the prevalence of diabetes in people aged over 20 years in Ahvaz, Iran. MATERIALS AND METHODS: The study population was chosen by cluster sampling. A checklist included: age, sex, weight, height, blood pressure, waist circumference, educational level, smoking status and previous history of diabetes was completed for each patient. Fasting Plasma Glucose (FPG) ≥126mg/dl and/or oral hypoglycemic treatment and/or insulin consumption was defined as diabetes, FPG=100-125mg/dl as Impaired Fasting Glucose (IFG) and FPG <100mg/dl as normal. RESULTS: Study population was 944 persons. Mean age of population was 42.2±14 years. Diabetes was detected in 15.1% of population. Only 40.4% of cases were aware of their disease. Diabetes was detected in 14.7% of female and 15.7% of male participants. Diabetes was related to age, waist circumference, family history of diabetes, hypertension, waist to hip ratio, educational level, marital status, serum triglyceride, cholesterol and body mass index (BMI) in both genders. But by using logistic regression analysis, age, family history of diabetes, hypertension, hypertriglyceridemia, and marital status had significant effect on diabetes. CONCLUSION: This study showed that using FPG criteria or current medication 15.1% of this population had diabetes and about 60% of patients were unaware of their disease. Age, hypertension, family history of diabetes, hypertriglyceridemia and marital status are the risk factors of diabetes in Ahvaz population. IFG have high prevalence and diabetes screening should be intensified in this population.

Risk of depressive symptoms associated with impaired glucose metabolism, newly diagnosed diabetes, and previously diagnosed diabetes: a meta-analysis of prospective cohort studies.

AIMS: Patients with diabetes had a higher risk of developing depressive symptoms. Little is known about the risk of depressive symptoms associated with different glucose metabolism status. We performed a meta-analysis of prospective cohort studies to investigate the risk of depressive symptoms among individuals with impaired glucose metabolism (IGM), newly diagnosed diabetes (NDM), and previously diagnosed diabetes (PDM), compared with those with normal glucose metabolism (NGM), and further examined the influence of diabetes-related comorbidities on the association. METHODS: PubMed and EMBASE were searched for relevant studies through 5 September 2015. The random-effects model was used to calculated overall relative risk (RR) and confidence interval (CI). Three separated meta-analyses were conducted by estimating the risk of depressive symptoms among people with IGM, NDM, and PDM, with NGM as a common reference category. Secondary analyses were conducted to examine whether adjustment for diabetes-related comorbidities affected the association. RESULTS: Five prospective cohort studies were included in the analyses, with a total of 18,051 participants involved. People with IGM (RR = 1.08, 95 % CI 0.84-1.38) and NDM (RR = 1.07, 95 % CI 0.74-1.55) were not associated with risk of developing depressive symptoms, whereas patients with PDM were associated with a modest increased risk of depressive symptoms (RR = 1.29, 95 % CI 1.03-1.63), after adjustment for demographic/socioeconomic factors. The risk of depressive symptoms associated with PDM was attenuated to be non-significant after pooling RRs that were adjusted for diabetes-related comorbidities. CONCLUSIONS: Our meta-analysis suggested people with PDM, but not IGM or NDM had an increased risk of developing depressive symptoms, and the risk was partially explained by diabetes-related comorbidities. Our findings indicated that routine diabetes care should put more emphasis on psychological problems of diabetic patients with complications.

Associations between Dietary Patterns and Impaired Fasting Glucose in Chinese Men: A Cross-Sectional Study.

Few studies have examined the association between Asian dietary pattern and prediabetes, in particular, the Chinese diet. We conducted a cross-sectional study to identify dietary patterns associated with impaired fasting glucose (IFG) which considered a state of prediabetes in Chinese men. The study included 1495 Chinese men aged 20 to 75 years. Information about diet was obtained using an 81-item food frequency questionnaire (FFQ), and 21 predefined food groups were considered in a factor analysis. Three dietary patterns were generated by factor analysis: (1) a vegetables-fruits pattern; (2) an animal offal-dessert pattern; and (3) a white rice-red meat pattern. The multivariate-adjusted odds ratio (OR) of IFG for the highest tertile of the animal offal-dessert pattern in comparison with the lowest tertile was 3.15 (95% confidence intervals (CI): 1.87-5.30). The vegetables-fruits dietary pattern was negatively associated with the risk of IFG, but a significant association was observed only in the third tertile. There was no significant association between IFG and the white rice-red meat pattern. Our findings indicated that the vegetables-fruits dietary pattern was inversely associated with IFG, whereas the animal offal-dessert pattern was associated with an increased risk of IFG in Chinese men. Further prospective studies are needed to elucidate the diet-prediabetes relationships.

Diet-induced obesity exacerbates metabolic and behavioral effects of polycystic ovary syndrome in a rodent model.

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy affecting women of reproductive age. Although a comorbidity of PCOS is obesity, many are lean. We hypothesized that increased saturated fat consumption and obesity would exacerbate metabolic and stress indices in a rodent model of PCOS. Female rats were implanted with the nonaromatizable androgen dihydrotestosterone (DHT) or placebo pellets prior to puberty. Half of each group was maintained ad libitum on either a high-fat diet (HFD; 40% butter fat calories) or nutrient-matched low-fat diet (LFD). Irrespective of diet, DHT-treated animals gained more body weight, had irregular cycles, and were glucose intolerant compared with controls on both diets. HFD/DHT animals had the highest levels of fat mass and insulin resistance. DHT animals demonstrated increased anxiety-related behavior in the elevated plus maze by decreased distance traveled and time in the open arms. HFD consumption increased immobility during the forced-swim test. DHT treatment suppressed diurnal corticosterone measurements in both diet groups. In parallel, DHT treatment significantly dampened stress responsivity to a mild stressor. Brains of DHT animals showed attenuated c-Fos activation in the ventromedial hypothalamus and arcuate nucleus; irrespective of DHT-treatment, however, all HFD animals had elevated hypothalamic paraventricular nucleus c-Fos activation. Whereas hyperandrogenism drives overall body weight gain, glucose intolerance, anxiety behaviors, and stress responsivity, HFD consumption exacerbates the effect of androgens on adiposity, insulin resistance, and depressive behaviors.

Changes in hippocampal synaptic functions and protein expression in monosodium glutamate-treated obese mice during development of glucose intolerance.

Glucose is the sole neural fuel for the brain and is essential for cognitive function. Abnormalities in glucose tolerance may be associated with impairments in cognitive function. Experimental obese model mice can be generated by an intraperitoneal injection of monosodium glutamate (MSG; 2 mg/g) once a day for 5 days from 1 day after birth. MSG-treated mice have been shown to develop glucose intolerance and exhibit chronic neuroendocrine dysfunction associated with marked cognitive malfunctions at 28-29  weeks old. Although hippocampal synaptic plasticity is impaired in MSG-treated mice, changes in synaptic transmission remain unknown. Here, we investigated whether glucose intolerance influenced cognitive function, synaptic properties and protein expression in the hippocampus. We demonstrated that MSG-treated mice developed glucose intolerance due to an impairment in the effectiveness of insulin actions, and showed cognitive impairments in the Y-maze test. Moreover, long-term potentiation (LTP) at Schaffer collateral-CA1 pyramidal synapses in hippocampal slices was impaired, and the relationship between the slope of extracellular field excitatory postsynaptic potential and stimulus intensity of synaptic transmission was weaker in MSG-treated mice. The protein levels of vesicular glutamate transporter 1 and GluA1 glutamate receptor subunits decreased in the CA1 region of MSG-treated mice. These results suggest that deficits in glutamatergic presynapses as well as postsynapses lead to impaired synaptic plasticity in MSG-treated mice during the development of glucose intolerance, though it remains unknown whether impaired LTP is due to altered inhibitory transmission. It may be important to examine changes in glucose tolerance in order to prevent cognitive malfunctions associated with diabetes.

Cognition in the Finnish diabetes prevention study.

We studied cognition in the Finnish Diabetes Prevention Study (DPS), a trial of lifestyle intervention that prevented diabetes in persons with impaired glucose tolerance. Cognition was similar in the randomization arms 9 years after the intervention in 364 participants, suggesting that the intervention did not benefit cognition.

Caracterización del metabolismo óseo mineral en pacientes con enfermedad renal crónica en hemodiálisis en el Servicio de Salud Metropolitano Sur, Santiago de Chile / Bone mineral metabolism in patients with chronic kidney disease on dialysis in Southern Metropolitan Santiago

Background: Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) is a condition of dialysis patients associated with both morbidity and mortality. Management is based on clinical guidelines with goals that are hard to comply with. Aim: To describe and compare biochemical variables associated with this disorder in two different time periods. Material and Methods: Revision of medical records of 814 patients (49% females) dialyzed during 2009 and 1018 patients (48% females), dialyzed during 2012 in Southern Metropolitan Santiago. Information about serum calcium, phosphorus, parathyroid hormone (PTH) and albumin was retrieved. Results: Median PTH values in 2009 and 2012 were 222.5 and 353.5 pg/ml respectively (p < 0.05). The figures for serum calcium corrected by albumin were 9.0 and 8.5 mg/dl respectively (p < 0.05). The figures for phosphorus were 4.7 and 5.0 mg/dl respectively (p < 0.05). The Calcium x Phosphorus product was 41.4 and 42.5 mg²/dl² (p < 0.05). Of note, the proportion patients with serum calcium below recommended levels (< 8.4 mg/dl) increased from 16% to 40% from 2009 to 2012. The proportion of patients with biochemical variables within recommended ranges was lower in 2012 than in 2009. Conclusions: There was a low proportion of patients with bone metabolism parameters within ranges recommended by clinical guidelines. These parameters were worst in 2012.

Associations of depression with impaired glucose regulation, newly diagnosed diabetes and previously diagnosed diabetes in Chinese adults.

AIM: To examine the association between depression and impaired glucose regulation, newly diagnosed diabetes and previously diagnosed diabetes in middle-aged and elderly Chinese people, and whether depression was associated with different treatment regimens or durations of diabetes. METHODS: A cross-sectional study was performed among 229,047 adults living in the community aged ≥ 40 years from 25 centres in China. The self-reported depression rating scale Patient Health Questionnaire 9 (PHQ-9) was used to diagnose probable and sub-threshold depression. Glucose metabolism status was determined according to World Health Organization 1999 diagnostic criteria. RESULTS: The numbers of participants with normal glucose regulation, impaired glucose regulation, newly diagnosed diabetes and previously diagnosed diabetes were 120,458, 59,512, 24,826 and 24,251, respectively. The prevalence of sub-threshold depression in the total sample of participants was 4.8% (4.8%, 4.8%, 4.4% and 5.6% from normal glucose regulation to previously diagnosed diabetes, respectively), and the prevalence of probable depression was 1.1% (1.1%, 1.0%, 0.9% and 1.8% from normal glucose regulation to previously diagnosed diabetes, respectively). Compared with participants with normal glucose regulation, those with previously diagnosed diabetes had increased odds of probable depression [odds ratio (OR) = 1.61, 95% confidence interval (CI) 1.39-1.87] and sub-threshold depression (OR = 1.14, 95% CI 1.06-1.24), after adjustment for multiple confounding factors. Newly diagnosed diabetes or impaired glucose regulation was not associated with depression. Among those with previously diagnosed diabetes, insulin treatment was associated with greater odds of depression compared with no treatment or oral anti-diabetic medicine. CONCLUSION: Previously diagnosed diabetes, but not newly diagnosed diabetes or impaired glucose regulation, was associated with a higher prevalence of depression. Patients receiving insulin were more likely to have depression than those not receiving treatment or being treated with oral anti-diabetic medicine.

Chronic variable stress improves glucose tolerance in rats with sucrose-induced prediabetes.

The incidence of type-2 diabetes (T2D) and the burden it places on individuals, as well as society as a whole, compels research into the causes, factors and progression of this disease. Epidemiological studies suggest that chronic stress exposure may contribute to the development and progression of T2D in human patients. To address the interaction between chronic stress and the progression of T2D, we developed a dietary model of the prediabetic state in rats utilizing unlimited access to 30% sucrose solution (in addition to unlimited access to normal chow and water), which led to impaired glucose tolerance despite elevated insulin levels. We then investigated the effects of a chronic variable stress paradigm (CVS; twice daily exposure to an unpredictable stressor for 2 weeks) on metabolic outcomes in this prediabetic model. Chronic stress improved glucose tolerance in prediabetic rats following a glucose challenge. Importantly, pair-fed control groups revealed that the beneficial effect of chronic stress did not result from the decreased food intake or body weight gain that occurred during chronic stress. The present work suggests that chronic stress in rodents can ameliorate the progression of diet-induced prediabetic disease independent of chronic stress-induced decreases in food intake and body weight.