Horses with high energy requirements are generally fed two large concentrate meals per day, either in the form of grain or pellets. The postprandial elevation of blood glucose resulting from this type of feeding has the potential to alter production of hormones such as leptin. Leptin is an adipose-derived protein that promotes satiety in normal animals. The objective of this study was to determine if feeding large amounts of concentrate twice each day would alter serum leptin concentration. Nine horses were placed into three groups (A, B, and C) and each group was rotated through three feeding schedules (2x, 3x, and 4x) in a 3 x 3 Latin square design. Horses were fed twice per day on the 2x schedule, three times per day on the 3x schedule, and four times per day on the 4x schedule. Horses were fed the same total amount of concentrate per day throughout the study, although meal size varied with the number of times the horse was fed per day. Horses were weighed and scored for body condition on the first day of each period. Each treatment period lasted for 11 days. Blood was drawn on days one, four, and seven of each period and leptin concentration was determined by radioimmunoassay. On the afternoon of the tenth day of each period, horses were fitted with jugular catheters and blood was drawn every two hours for 24-hours to determine the circadian rhythm of leptin secretion. Additionally, blood was taken 30 minutes prior to and every 30 minutes after the morning meal to determine postprandial plasma glucose concentrations. Mean and peak glucose values were higher on the 2x schedule than the 3x or 4x schedules (P < 0.05). Leptin concentration was highest in horses on the 3x schedule, although when these data were normalized to baseline (day one) values, leptin was highest on the 2x schedule (P < 0.05). Serum leptin concentration was highly correlated with body condition score (P < 0.01), but not gender (P = 0.82), and leptin increased throughout the study (P < 0.05). Data from the 24-hour collection showed that serum leptin concentration varied with time in horses on the 2x but not the 4x schedule (P < 0.05). Linear regression of data from the 2x schedule indicates that the pattern of change may be modeled by a quadratic equation (P < 0.05). This study demonstrates that feeding horses large carbohydrate meals twice per day disrupts the normal pattern of leptin in the horse, possibly affecting appetite and other physiological processes.

Horses with high energy requirements are generally fed two large concentrate meals per day, either in the form of grain or pellets. The postprandial elevation of blood glucose resulting from this type of feeding has the potential to alter production of hormones such as leptin. Leptin is an adipose-derived protein that promotes satiety in normal animals. The objective of this study was to determine if feeding large amounts of concentrate twice each day would alter serum leptin concentration. Nine horses were placed into three groups (A, B, and C) and each group was rotated through three feeding schedules (2x, 3x, and 4x) in a 3 x 3 Latin square design. Horses were fed twice per day on the 2x schedule, three times per day on the 3x schedule, and four times per day on the 4x schedule. Horses were fed the same total amount of concentrate per day throughout the study, although meal size varied with the number of times the horse was fed per day. Horses were weighed and scored for body condition on the first day of each period. Each treatment period lasted for 11 days. Blood was drawn on days one, four, and seven of each period and leptin concentration was determined by radioimmunoassay. On the afternoon of the tenth day of each period, horses were fitted with jugular catheters and blood was drawn every two hours for 24-hours to determine the circadian rhythm of leptin secretion. Additionally, blood was taken 30 minutes prior to and every 30 minutes after the morning meal to determine postprandial plasma glucose concentrations. Mean and peak glucose values were higher on the 2x schedule than the 3x or 4x schedules (P < 0.05). Leptin concentration was highest in horses on the 3x schedule, although when these data were normalized to baseline (day one) values, leptin was highest on the 2x schedule (P < 0.05). Serum leptin concentration was highly correlated with body condition score (P < 0.01), but not gender (P = 0.82), and leptin increased throughout the study (P < 0.05). Data from the 24-hour collection showed that serum leptin concentration varied with time in horses on the 2x but not the 4x schedule (P < 0.05). Linear regression of data from the 2x schedule indicates that the pattern of change may be modeled by a quadratic equation (P < 0.05). This study demonstrates that feeding horses large carbohydrate meals twice per day disrupts the normal pattern of leptin in the horse, possibly affecting appetite and other physiological processes.

Background/Aim: Hepatitis C virus infection is a known risk factor of impaired glucose metabolism and diabetes mellitus. Whether hepatitis B virus (HBV) infection is also associated with impaired glucose tolerance remains uncertain. The aim of the study was to conduct a systematic review on the association between HBV infection and impaired glucose metabolism Methods: Studies reporting the association between HBV infection and markers of impaired glucose metabolism were identified through keyword search in PubMed and Google Scholar. 10 studies (out of 320) were included in this systematic review. Results were included. Majority (n=7) of the included studies were conducted among the Asian populations. Of the 10 included studies, eight studies reported a significant association between HBV infection and impaired glucose metabolism, proxied by impaired glucose tolerance, impaired fasting glucose, diabetes mellitus, insulin resistance, and metabolic syndromes. The remaining two studies using diabetes mellitus and insulin resistance as outcome measures did not find a positive association with HBV infection. Conclusions: The association between HBV and impaired glucose metabolism is suggestive from the evidence compiled from included articles. However, whether the development of glucose intolerance or diabetes mellitus is linked to an infectious cause of HBV is still inconclusive. Further studies that could improve on the current understanding of the associations between HBV infection and impaired glucose metabolism are necessary. / published_or_final_version / Public Health / Master / Master of Public Health

Mammals have to adapt quickly to the changes of nutrition availability. The liver is the central organ that coordinates the responses to food deprivation upon fasting and nutrient overload during feeding. In liver, hormonal and nutrient pathways converge into the regulation of transcriptional programs that are involved in maintaining energy homeostasis. When these fine-tuned regulations in liver are altered due to constant surplus of nutrients or insufficient hormonal actions, multiple metabolic diseases including type II diabetes can occur, followed by severe complications. As a part of those regulatory programs, PGC-1alpha (peroxisome proliferator-activated receptor gamma coactivator-1alpha) links hormonal signaling to the expression of glucose and lipid metabolic genes. Its transcriptional co-activator activity is tightly controlled via post-translational modification; GCN5 (histone acetyltransferase KAT2A) acetylates PGC-1alpha and suppresses its transcriptional activity, whereas Sirt1 deacetylates and activates PGC-1alpha. Herein, cyclin D1-CDK4 (cyclin-dependent kinase 4) kinase is identified as a new regulator of glucose metabolism in liver that modulates PGC-1alpha's transcriptional activity. Through a cell-based high throughput chemical screen, a CDK4 inhibitor was discovered to potently decrease PGC-1alpha acetylation. Cyclin D1-CDK4 kinase phosphorylates and activates GCN5, which then acetylates and inhibits PGC-1alpha activity on hepatic gluconeogenic genes. Feeding activates cyclin D1-CDK4 kinase in liver, which, in turn, suppresses glucose production independently of cell cycle progression. As part of the feeding response, insulin/GSK3beta (glycogen synthase kinase 3beta) signaling stabilizes cyclin D1 protein via sequestering cyclin D1 in the nucleus. In parallel, dietary amino acids increase hepatic cyclin D1 mRNA transcripts. Loss of hepatic cyclin D1 in mice leads to mild diabetic phenotypes. In diabetic models, cyclin D1-CDK4 is chronically elevated and refractory to fasting/feeding transitions; nevertheless further activation of this kinase normalizes glycemia. Thus, these findings show that hormonal and nutrient pathways utilize components of the cell cycle machinery in post-mitotic cells to control glucose homeostasis independently of cell cycle progression. / Chemistry and Chemical Biology

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To study maternal glucose tolerance in pregnancy and its effects on the fetus, a rapid 25g intravenous glucose tolerance test was performed at about 32 weeks gestation in a group of randomly selected women. Full glucose tolerance data was available in 815 cases. The results were withheld from the patients and their obstetricians and paediatricians, and no treatment or advice was offered. Fasting plasma glucose and indices of glucose disposal were distributed unimodally with no evidence of a separate pathological group towards the diabetic end of the distributions. Glucose disposal rate was not, however, signficantly associated with the fasting plasma glucose, suggesting that glucose intolerance associated with elevation of the fasting plasma glucose might be a more clearly defined entity. New reference standards for fasting plasma glucose in pregnancy, which differ from those currently in use, are presented. The major determinants of relatively impaired maternal glucose tolerance in pregnancy were maternal age and obesity. Nonetheless, many cases of relative glucose intolerance occurred in the absence of any preexisting clinical indication. Significant association were found between maternal glucose metabolism and various measures of neonatal size and morbidity, including the incidence of congenital malformations and the occurrence of perinatal asphyxia in post-term infants. These effects were graded through much of the range of maternal glucose tolerance and not of predictive value in individual cases. The available evidence did not indicate that these relationships were mediated by fetal hyperinsulinism. It is concluded that the adverse consequences of impaired glucose disposal with normal fasting plasma glucose in pregnancy do not justify exhaustive measures to identify the condition. Screening for glucose intolerance during pregnancy should seek to identify those cases in which glucose intolerance is associated with elevation of fasting plasma glucose.

No description available.