Relatively little is known about how the diet of chronically undernourished children may impact cardiometabolic biomarkers. The objective of this exploratory study was to characterise relationships between dietary patterns and the cardiometabolic profile of 153 3-5-year-old Peruvian children with a high prevalence of chronic undernutrition. We collected monthly dietary recalls from children when they were 9-24 months old. At 3-5 years, additional dietary recalls were collected, and blood pressure, height, weight, subscapular skinfolds and fasting plasma glucose, insulin and lipid profiles were assessed. Nutrient intakes were expressed as average density per 100 kcals (i) from 9 to 24 months and (ii) at follow-up. The treelet transform and sparse reduced rank regress\'ion (RRR) were used to summarize nutrient intake data. Linear regression models were then used to compare these factors to cardiometabolic outcomes and anthropometry. Linear regression models adjusting for subscapular skinfold-for-age Z-scores (SSFZ) were then used to test whether observed relationships were mediated by body composition. 26 % of children were stunted at 3-5 years old. Both treelet transform and sparse RRR-derived child dietary factors are related to protein intake and associated with total cholesterol and SSFZ. Associations between dietary factors and insulin were attenuated after adjusting for SSFZ, suggesting that body composition mediated these relationships. Dietary factors in early childhood, influenced by protein intake, are associated with cholesterol profiles, fasting glucose and body fat in a chronically undernourished population.

UNASSIGNED: Cirrhosis of liver is associated with loss of liver function, portal hypertension, and pancreatic β-cell dysfunction leading to hepatogenous diabetes (HD). Often HD is an underestimated and understudied problem, particularly in the Indian subcontinent, where the prevalence of both Chronic liver disease (CLD) and diabetes is high. Hence this study was planned to highlight the prevalence of HD and its association with the severity of cirrhosis.
UNASSIGNED: A total of 121 cirrhotic patients without a history of diabetes were included in this prospective cross-sectional study. Seventy five g oral glucose tolerance test (OGTT) was done in all patients. Fasting serum insulin levels were done to calculate insulin resistance (IR) using homeostatic model assessment-insulin resistance (HOMA-IR). Upper gastrointestinal endoscopy was done to detect varices. Patients were divided into HD group and non-HD group for comparison of results.
UNASSIGNED: HD was seen in 52 (42.98%) patients; among them, 63.4% did not show evidence of HD by fasting plasma glucose (FPG) levels. Impaired glucose tolerance (IGT) was seen in 58 (47.93%) patients. Compared with the non-HD group, the HD group had significantly higher model for end-stage liver disease (MELD) score (P = 0.038), HOMA-IR (P < 0.001), incidence of large varices (P < 0.001) and variceal bleeding (P < 0.001). A statistically significant association was noted between HD and Hepatocellular carcinoma (HCC) (P < 0.001).
UNASSIGNED: Patients with cirrhosis had a high prevalence of IGT, IR, and HD. The presence of HD is well associated with the severity of cirrhosis in the form of higher MELD score (>15), CTP score (>10), higher bilirubin levels, large varices, bleeding varices, and HCC. FPG levels and glycated hemoglobin (HbA1c) cannot be relied upon, and OGTT aids in the unmasking of HD in these patients.

Elevated serum ferritin has been linked to type 2 diabetes (T2D) and adverse health outcomes in subjects with the Metabolic Syndrome (MetS). As the mechanisms underlying the negative impact of excess iron have so far remained elusive, we aimed to identify potential links between iron homeostasis and metabolic pathways.
In a cross-sectional study, data were obtained from 163 patients, allocated to one of three groups: (1) lean, healthy controls (n = 53), (2) MetS without hyperferritinemia (n = 54) and (3) MetS with hyperferritinemia (n = 56). An additional phlebotomy study included 29 patients with biopsy-proven iron overload before and after iron removal. A detailed clinical and biochemical characterization was obtained and metabolomic profiling was performed via a targeted metabolomics approach.
Subjects with MetS and elevated ferritin had higher fasting glucose (p < 0.001), HbA1c (p = 0.035) and 1 h glucose in oral glucose tolerance test (p = 0.002) compared to MetS subjects without iron overload, whereas other clinical and biochemical features of the MetS were not different. The metabolomic study revealed significant differences between MetS with high and low ferritin in the serum concentrations of sarcosine, citrulline and particularly long-chain phosphatidylcholines. Methionine, glutamate, and long-chain phosphatidylcholines were significantly different before and after phlebotomy (p < 0.05 for all metabolites).
Our data suggest that high serum ferritin concentrations are linked to impaired glucose homeostasis in subjects with the MetS. Iron excess is associated to distinct changes in the serum concentrations of phosphatidylcholine subsets. A pathway involving sarcosine and citrulline also may be involved in iron-induced impairment of glucose metabolism.

BACKGROUND: Turner syndrome (TS) is the most common chromosomal abnormality in females and is associated with several co-morbidities. It commonly results from X monosomy which is diagnosed on a 30 cell karyotype. Congenital heart disease is a clinical feature in 30% of cases. It is becoming evident that TS patients have an increased risk of cardiovascular and cerebrovascular diseases.
METHODS: This review provides a detailed overview of the literature surrounding cardiometabolic health in childhood and adolescent TS. In addition, the review also summarises the current data on the impact of growth hormone (GH) therapy on cardiometabolic risk in paediatric TS patients.
CONCLUSIONS: Current epidemiological evidence suggests that young women and girls with TS have unfavourable cardiometabolic risk factors which predispose them to adverse cardiac and cerebrovascular outcomes in young adulthood. It remains unclear whether this risk is the result of unidentified factors which are intrinsic to TS, or whether modifiable risk factors (obesity, hypertension, hyperglycaemia) are contributing to this risk.
CONCLUSIONS: From a clinical perspective, this review highlights the importance of regular screening and pro-active management of cardiometabolic risk from childhood in TS cohorts and that future research should aim to address whether modification of these variables at a young age can alter the disease process and atherosclerotic outcomes in adulthood.