Puberty and type 1 diabetes Chowdhury, Subhankar
Indian journal of endocrinology and metabolism,
04/2015, Letnik:
19, Številka:
Suppl 1
Journal Article
Recenzirano
Odprti dostop
Various data on type 1 diabetes mellitus (T1DM) have showed that the incidence of T1DM peaks at puberty. However, diabetes control and complications could be adversely affected by the physiological ...changes of puberty. In early years of insulin therapy, severe growth retardation with pubertal delay, like in Mauriac syndrome, have been reported. Insulin and leptin are metabolic factors, circulating in the periphery, which participate in the hypothalamic control of metabolism and reproduction. Insulin may be an important regulator of leptin in humans. Increased levels of advanced glycation end products suppress activation of the gonadotropin-releasing hormone (GnRH) pulse generator, resulting in pubertal delay. Glycemic control deteriorates during puberty as the lean body mass doubles mainly over a period of 25 years, which increases insulin requirement. There is also an increase in insulin resistance over the period of puberty. In normal individuals, fasting and postprandial insulin concentrations reach a peak in both sexes in mid to late puberty. Puberty, at all stages, has the worst insulin resistance. It has been observed that an excessive GH secretion in T1DM during puberty has significant effects on ketogenesis. Adolescent T1DM tends to decompensate very rapidly and develop ketoacidosis when the late night insulin dose is omitted. Adolescence is a critical developmental phase that presents unique challenges and opportunities to individuals with diabetes, their families and their healthcare providers.
Background
Coronavirus disease 2019 (COVID-19) has aroused global health concerns, particularly in relation to diabetes where it has been associated with poorer outcomes. The bulk of the evolving ...evidence in diabetes and COVID-19 relates to type 2 diabetes (T2D). Since there are a significant number of patients with type 1 diabetes (T1D) with unique concerns and challenges during the ongoing COVID-19 pandemic, we reviewed existing literature, relevant websites, and related guidelines to form this narrative review to help address key questions in this area.
Methods
We systematically searched the PubMed database up to May 31, 2020, and retrieved all the articles published on T1D and COVID-19.
Results
We found 18 relevant articles, each of which carried a part of the evidence regarding the risk of contracting COVID-19 in patients with T1D, effect of COVID-19 on development of T1D, outcomes in T1D with COVID-19, and special management issues in T1D in the light of COVID-19. These have been documented in the present review.
Conclusion
COVID-19 with T1D presents special challenges. While the available evidence does shed some light, we need more evidence to deal with this difficult duo.
The sharp inclination in the emissions from conventional vehicles contribute to a significant increase in environmental issues, besides the energy crises and low conversion efficiency leads to the ...evolution of electric vehicles (EV). Hybrid electric vehicles (HEV) have efficient fuel economy and reduce the overall running cost, but the ultimate goal is to shift completely to the pure electric vehicle. Despite this, the main obstruction of HEV is energy storage capability. An EV requires high specific power (W/kg) and high specific energy (W·h/kg) to increase the distance travelled and reduce the time required for charging. The main focus of this paper is on the energy sources as these are the main components in EVs towards making them eco-friendly and cost-effective. Various topologies of EV technology such as HEVs, plug-in HEVs, and many more have been discussed. These topologies of EVs are based on the diverse combination of batteries, fuel cells, super-capacitor, flywheels, regenerative braking systems, which are used as energy sources and energy storage devices.
•A review on various topologies of electric vehicle based on energy sources.•An overview on operating principles of energy storage system with its management.•An overview on challenges involved in adaptation of energy storage system.
Type 2 diabetes mellitus (T2DM) accompanied by hyperlipidemia confers higher risk for diabetes as well as cardiovascular diseases. NF-κB is actively involved in generating low-grade inflammation and ...oxidative stress triggering the development of diabetic complications. In this study, we have attempted to investigate the association between NF-κB1 functional promoter polymorphism-94 ATTG insertion/deletion (rs28362491) with inflammatory markers in developing diabetes-linked dyslipidemia. We performed a case–control study in a total of 401 individuals belonging to three categories such as Type 2 diabetes with dyslipidemia, Type 2 diabetes without dyslipidemia, and normal healthy controls. Experiments were carried out using genotyping, real-time PCR, and western blot. Pearson’s correlation, analysis of variance, and logistic regression were utilized for statistical analysis. As per genetic association conducted in this study the SNP rs28362491 showed significant allelic and genotypic associations (Allelic: OR = 1.374, CI 0.9797–1.927
,
p
= 0.003, and Genotypic in dominant model: OR = 1.77, CI 1.04–2.99,
p
= 0.002) with the risk of diabetes and associated dyslipidemia. The -94 ATTG insertion/insertion (ins/ins) genotype was associated with significantly increased level of serum TNF-α (
p
= 0.002), serum IL-6 (
p
= 0.067) in diabetes-induced dyslipidemia. Multiple linear regression analysis identifies independent correlation of Total cholesterol, HDL, LDL, TNF-α, and rs28362491 ATTG ins/ins with triglyceride in diabetic dyslipidemic condition. T2DM with dyslipidemia having ins/ins genotype showed significant increased expression of pro-inflammatory cytokines such as TNF-α, IL-6, and activation of NF-κB. Our study reports that individuals with ATTG insertion allele and ATTG ins/ins genotype at NF-κB1 promoter regulatory gene predicts the risk and severity of T2DM-linked dyslipidemia.
Type 2 diabetes (T2D) is a serious public health issue and may also contribute to modification in the structure of the intestinal microbiota, implying a link between T2D and microbial inhabitants in ...the digestive tract. This work aimed to develop efficient models for identifying essential physiological markers for improved T2D classification using machine learning algorithms. Using amplicon metagenomic approaches, an effort has also been made to understand the alterations in core gut microbial members in Indian T2D patients with respect to their control normal glucose tolerance (NGT). Our data indicate the level of fasting blood glucose (FBG) and glycated hemoglobin (HbA1c) were the most useful physiological indicators while random forest and support vector machine with RBF Kernel were effective predictions models for identifications of T2D. The dominating gut microbial members
Allopreotella, Rikenellaceae RC9 gut group, Haemophilus, Ruminococcus torques group
, etc. in Indian T2D patients showed a strong association with both FBG and HbA1c. These members have been reported to have a crucial role in gut barrier breakdown, blood glucose, and lipopolysaccharide level escalation, or as biomarkers. While the dominant NGT microbiota (
Akkermansia, Ligilactobacillus, Enterobacter
, etc.) in the colon has been shown to influence inflammatory immune responses by acting as an anti-inflammatory agent and maintaining the gut barrier. The topology study of co-occurrence network analysis indicates that changes in network complexity in T2D lead to variations in the different gut microbial members compared to NGT. These studies provide a better understanding of the gut microbial diversity in Indian T2D patients and show the way for the development of valuable diagnostics strategies to improve the prediction and modulation of the T2D along with already established methods.
Increasing burden of non-communicable diseases like diabetes and cardiovascular disorders has made the global health scenario more challenging. Dyslipidemia in diabetes is a compounding risk factor ...for cardiovascular diseases, but there is dearth of identifying appropriate signatures to address this issue. The protein, adiponectin, is actively involved in regulating glucose levels as well as fatty acid breakdown playing crucial role in dyslipidemia and vascular complications. To identify the underlying genetic and molecular profile of adiponectin metabolic pathway in diabetic dyslipidemia and to correlate it with known biochemical and oxidative stress parameters of T2DM, we performed a case–control study in a total 264 individuals belonging to three categories such as diabetes with dyslipidemia (
n
= 88), diabetes without dyslipidemia (
n
= 86) and normal healthy controls (
n
= 90). Expression of adiponectin (ADIPOQ) and its receptors (ADIPOR1 and ADIPOR2) were measured in visceral and subcutaneous adipose tissues. A significant downregulated expression of ADIPOQ and its receptors in adipose tissues and PBMCs were linked with diabetic dyslipidemic condition. A multiple linear regression followed by MDR analysis implicated the elevated plasma malondialdehyde and decreased adiponectin level to be correlated with diabetic dyslipidemia. More interestingly, two single nucleotide polymorphisms of ADIPOQ (rs2241766 and rs1501299) were genetically associated with the risk of developing dyslipidemia. Other important biochemical factors found to be increased in diabetic dyslipidemic conditions included plasma C-reactive protein and 4-hydroxynonenal adducts. Our results explore, a complex interplay of genetic and biochemical parameters in diabetic dyslipidemia which is significant from the perspective of risk stratification and novel therapeutic strategy development.
Objective
Non-obese type 2 diabetes seems to be common in India; hence the current study tried to understand the pathogenesis of diabetes in this group focusing on the role of adipocytes especially ...abdominal fat compartment. Comparison was made between non-obese subjects with newly detected diabetes and those without diabetes, in relation to levels of adipogenic factor and adipokines in pre-adipocytes and mature adipocytes respectively.
Research design methods
Non-obese subjects (BMI-18–25 Kg/m
2
) were consecutively selected of whom 15 had newly-detected, treatment naïve type 2 diabetes (HbA1% ≥6.5) while 25 were control (HbA1c% ≤5.6). We examined the expression of adipocyte differentiation factor – SREBP-1c from preadipocytes and adipocyte specific adipokines- HMW isoform and total adiponectin, leptin, FABP-4, TNF-α and IL-6 from adipocytesisolated from abdominal visceral and subcutaneous adipose tissues (VAT and SCAT) by RT-PCR and as well as from serum by ELISA. Size of cultured adipocytes was measured in a fully automated imaging system microscope.
Result
Both in SCAT and VAT, SREBP-1c and adiponectin had significantly lower expression along with increased mRNA level of inflammatory adipokinesdiabetes.Average adipocyte size and frequency of large(hypertrophied) adipocytes were comparatively higher in T2DM subjects and had significant negative correlation with SREBP-1c. HMW adiponectin level significantly reduced in the secretion from VAT and SCAT of T2DM subjects compared to control.
Conclusion
Reduced expression of SREBP-1c in preadipocytes may lead to increased number of hypertrophied adipocytes in T2DM. Therefore, these dysfunctional hypertrophied adipocytes could cause imbalanced expression of insulin resistant and insulin sensitive adipokines.
Purpose
Baseline renal dysfunction predicts mortality in primary hyperparathyroidism (PHPT). However, it remains controversial whether renal insufficiency in PHPT is due to disease severity alone or ...other risk factors. This study aimed to explore the association of clinico-biochemical variables with renal dysfunction estimated glomerular filtration rate (eGFR) < 60 ml/min/m
2
in PHPT.
Methods
A total of 112 patients of PHPT were selected and divided into following subgroups: renal dysfunction (n = 28) and normal renal function (n = 84). Demographic characteristics, traditional risk factors, phenotypes of PHPT based on target organ involvement, and biochemical parameters were compared between these subgroups.
Results
Patient subgroups of PHPT with and without renal dysfunction had similar age, frequency of diabetes, and hypertension. Renal dysfunction was more prevalent in males (p < 0.05). Compared to normal renal function subgroup, individuals with renal dysfunction had higher serum levels of calcium, phosphate, alkaline phosphatase, intact parathormone (all p < 0.05), while having lower hemoglobin levels (p < 0.05) and higher nephrolithiasis rates (p < 0.05). Multiple regression analysis revealed that nephrolithiasis, serum calcium-phosphorous product (CaxP), parathormone levels were positively associated with baseline renal dysfunction (all p < 0.01). A baseline PTH > 456 pg/mL and CaxP > 30.0 mg
2
/dl
2
could discriminate renal dysfunction from normal renal function with sensitivity and specificity of 75% and 74.5% and 92.6% and 74.4%, respectively.
Conclusion
Renal dysfunction was associated with presence of nephrolithiasis, elevated serum CaxP and PTH levels in our cohort with predominantly symptomatic PHPT, indicating an association with the underlying disease itself. Serum CaxP may additionally be appraised during risk assessment in PHPT.
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