Our findings suggest that circulating ferritin levels may serve as a predictor of T2D risk in a sex-specific manner. Assessment of HV and psychopathology in patients with CS revealed no reduction of HV, but cognition, depressive symptoms, and quality of life were substantially affected.
Sleep is essential for healthy living. Establishing the effect of abnormal sleep on andrological issues will promote prioritization of sleep, and may thereby improve overall long-term health outcomes. This article explores how pubertal timing affects adult outcomes by reviewing findings from Mendelian randomization studies and studies of sex-steroid treatment of adolescent hypogonadal conditions.
The endocannabinoid system participates in bone growth and remodeling. Increasing use of medical cannabis makes the role of the endocannabinoid system in bone biology clinically important. Overweight and obesity are often encountered in fracture cases. The presumed protective effect of overweight and obesity on bone fragility should be reconsidered. This mini-review offers a comprehensive description of the current pathophysiology, immunology, and clinical spectrum of the complex autoimmune polyendocrinopathy syndrome, as well as a synopsis of recent and novel reports.
To prevent premature cardiovascular disease and promote life-long heart-healthy living in children and adolescents, additional training is needed for pediatric endocrinologists.
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Hemodynamic and systemic vascular effects of dapagliflozin undergo epigenetic regulation that favorably affects two miRs involved in heart failure. However, the outcomes in the HST group were worse. Of 33 children with severe FSS, the genetic etiology was elucidated in Half of the causative variants affect the growth plate. Growth plate disorders are a prevalent cause of FSS. Among pregnant US women, we found higher copper and lower molybdenum could potentially increase the risk of glucose dysregulation, with those at higher risk of GDM affected to a greater extent.
This study uses pharmacologic probes to demonstrate that endogenous GnRH-induced LH pulses can be generated in the absence of neurokinin B and dynorphin activity in humans and mice. We propose using the combined evaluation of maximum serum total and salivary cortisol responses after low-dose ACTH to test for central adrenal insufficiency in pediatric patients. Our data suggest that the multistep biochemical testing for diagnosis of subclinical Cushing syndrome could be simplified by a single test of plasma levels of multiple steroids.
This study provides normative sensor glucose data in a healthy, nondiabetic population of children and adults. However, pre-neoplasia and ongoing spermatogenesis are both relatively common in all patients. Apparently nonfunctioning adrenal tumors in patients with nonlateralized hyperaldosteronism exhibit latent autonomous cortisol secretion leading to high prevalences of diabetes and proteinuria. Study assessed sex differences in effects of obesity on reproductive hormones in early puberty and found that obesity has differential effects on reproductive hormones in girls and boys.
Children with type 1 diabetes were randomized to a placebo or prebiotic group. The prebiotic group showed significantly higher C-peptide and increased relative abundance of Bifidobacterium. In postmenopausal women, the degree of unsuppressed glucocorticoid secretion and peripheral activation and sensitivity is associated with the presence of hypertension.
In this population study, galectin-3 was associated with prevalent and incident diabetes independent of traditional risk factors. The long-term benefit of surgery in this population is unknown.
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The concept of energy turnover was used to show that a physical activity level of 1. This increased postprandial lipemia is especially marked in women, who generally have less postprandial lipemia than men. Chylomicron clearance requires several steps Fig. The particle then interacts with LpL on capillary lumenal endothelial cells of cardiac and skeletal muscle and adipose tissue. Released fatty acids are taken up by those tissues, perhaps via the fatty acid transporter, CD36 25 , and a smaller triglyceride-depleted particle, a chylomicron remnant, is created.
Chylomicrons contain a truncated form of apoB termed apoB A correlation between postprandial lipemia and atherosclerosis has been found in a number of clinical studies In addition, apoB48 remnants are found in a number of atherogenic animal models made with diets and genetic modifications 27 , It is generally accepted that remnant lipoproteins, in addition to LDL, are atherogenic. Effects of diabetes on postprandial lipemia.
A defect in removal of lipids from the bloodstream after a meal is common in patients with diabetes. Chylomicron metabolism requires that these lipoproteins obtain apoCII after they enter the bloodstream from the thoracic duct. Triglyceride within the particles can then be hydrolyzed by LpL, which is found on the wall of capillaries. LpL activity is regulated by insulin, and its actions are decreased in diabetes.
Triglyceride-depleted remnant lipoproteins are primarily degraded in the liver. Because remnants contain a truncated form of apoB, apoB48, that does not interact with these receptors, this uptake is mediated by apoE. Remnant lipoproteins can be removed from the bloodstream via several pathways, some of which appear to be modulated by diabetes.
Liver is the major, although not exclusive, site of remnant clearance. As these particles percolate through the liver, they are trapped by association with the negatively charged proteoglycans within the space of Disse. This process may be aided by the presence of apoE and hepatic lipase, proteins that bind to both lipid particles and proteoglycans.
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Both hepatic lipase and heparan sulfate proteoglycan production 29 may be reduced in diabetes. The second step in remnant clearance is via cellular internalization and degradation of the particles. Some of the remnants may be directly internalized along with cell surface proteoglycans. Most remnant uptake is via receptors.
In very poorly controlled diabetes LDL receptors may be decreased. Although most patients with poorly controlled diabetes develop hypertriglyceridemia, occasional patients develop severe hyperchylomicronemia. At higher levels the patients can develop eruptive xanthomas, lipemia retinalis, and pancreatitis. Most of these patients have an underlying lipid disorder, such as heterozygous LpL deficiency, that is then exacerbated by diabetes The relationship between severe hypertriglyceridemia and diabetes is sometimes obscured because primary LpL deficiency can lead to recurrent pancreatitis and insulin deficiency.
In contrast to this, recent experimental data have shown that the LpL is expressed in the islet cells, and it has been postulated that this enzyme may promote fat-induced toxicity leading to defective insulin secretion Increased plasma VLDL. Patients with diabetes, especially type 2 diabetes, have increased VLDL production 1. Insulin infusion will correct this abnormality 7 either because of the concomitant reduction in plasma fatty acids or because of direct effects of insulin on the liver Fig.
Effects of diabetes on VLDL production. Poorly controlled type 1 diabetes and type 2 diabetes are associated with increased plasma levels of VLDL. Two factors may increase VLDL production in the liver: the return of more fatty acids due to increased actions of hormone-sensitive lipase HSL in adipose tissue and insulin actions directly on apoB synthesis. Both of these processes will prevent the degradation of newly synthesized apoB and lead to increased lipoprotein production. VLDL, like chylomicrons, requires LpL to begin its plasma catabolism, leading to the production of LDL or the return of partially degraded lipoprotein to the liver.
Both the composition and the size of VLDL determine its metabolic fate.
In diabetes greater amounts of fatty acids returning to the liver are reassembled into triglycerides and secreted in VLDL. A greater content of triglyceride leads to the production of larger particles. A greater proportion of large lighter VLDL return to the liver without complete conversion to LDL 33 ; this pathway is akin to that of chylomicrons.
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Like chylomicrons, apoE may be the ligand that mediates liver uptake of these particles. Thus, VLDL metabolism is a competition between liver uptake of partially catabolized lipoproteins and intracapillary lipolysis, a process that may require several steps to complete VLDL conversion to LDL. LDL are not usually increased in diabetes.
In part this may represent a balance of factors that affect LDL production and catabolism. Conversely, increases in this lipolytic step that accompany weight loss, fibric acid drug therapy, and treatment of diabetes may increase LDL levels. Occasionally diabetic patients, especially those with very poor glycemic control, may have increased LDL that is reduced by treatment of their diabetes. This is due to effects on either the LDL or the receptor. Increased small dense LDL. Heterogeneity exists in the size and composition of all classes of lipoproteins.
The ratio of lipid to denser protein varies, and this determines both the buoyancy and the size of the particle, as the lipids are primarily contained in the core. The core of all lipoproteins contains hydrophobic cholesteryl ester and triglyceride. In the absence of a defect in these enzymes, lipoproteins enriched in triglyceride will be converted to small, denser forms.
Plasma lipid exchange. This triglyceride can then be converted to free fatty acids by the actions of plasma lipases, primarily hepatic lipase. A decrease in the size and an increase in density of LDL are characteristic of most hypertriglyceridemic states, including diabetes. Because of this, small dense LDL is considered by many to be one of the hallmarks of diabetic dyslipidemia rather than the expected companion of reduced HDL and increased triglyceride levels 2.
The special designation given to LDL size, rather than HDL and VLDL size, is based on a large amount of clinical and experimental data implying that these particles confer additional atherosclerotic risk. In vitro , small dense LDL can be oxidized more easily, the particles do not interact with LDL receptors as well, and they may associate with proteoglycans on the surface of cells or in matrix more readily.follow site
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Although several human studies imply that small dense LDL are an additional marker for atherosclerosis development 34 , this observation may be restricted to patients with increased levels of apoB and decreased HDL In other studies the concomitant association of hypertriglyceridemia and low HDL appears to obscure any additional risk profiling attributable to LDL size In dietary studies using primates, larger, not smaller, LDL size correlates with atherosclerosis, presumably because each of these LDL carries more cholesterol This can be done by measuring LDL density using an ultracentrifuge or by measuring size using gradient gels or light scattering.
Another method of determining the likelihood of a patient having small dense LDL is by waist measurement, a cheaper and easier test 38 , Obesity and insulin resistance are highly correlated with small dense LDL. Reduced HDL. There are several reasons for the decrease in HDL found in patients with diabetes Fig. Clinical measurements of HDL are of HDL cholesterol; therefore, substitution of triglyceride for cholesteryl ester in the core of the particle leads to a decrease in this measurement. Moreover, the triglyceride, but not cholesteryl ester, in HDL is a substrate for plasma lipases, especially hepatic lipase that converts HDL to a smaller particle that is more rapidly cleared from the plasma This increases HDL lipid content.
Defective lipolysis leads to reduced HDL production. Effects of diabetes on HDL metabolism. HDL production requires the addition of lipid to small nascent particles. A second pathway is via efflux of cellular free cholesterol FC , a process that involves the newly described ABC1 transporter and esterification of this cholesterol by the enzyme lecithin cholesterol acyl transferase LCAT.
HDL catabolism may occur through several steps.
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Hepatic lipase and scavenger receptor-BI are found in the liver and in steroid-producing cells. In contrast, the kidney degrades HDL protein apoAI without lipid, perhaps by filtering nonlipid-containing protein. Within the last 2 yr a number of additional enzymes and receptors have been discovered that are integral regulators of HDL metabolism and presumably the effects of HDL on atherosclerosis. It is not yet clear whether hyperglycemia or insulin is an important regulator of these molecules.
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