Introduction: This review paper aims to discuss the effects of insulin resistance, and its association with various metabolic diseases. Insulin resistance (IR), characterized by diminished tissue ...responsiveness to physiological insulin levels, is a key component in various metabolic diseases, including type 2 diabetes, cardiovascular disorders (CVDs), obesity, and non-alcoholic fatty liver disease (NAFLD). State of knowledge The consequences of IR are profound; in type 2 diabetes, it hinders glucose utilization by muscle cells, leading to hyperglycemia, muscle damage, and loss of mass and strength. IR also plays a central role in NAFLD, promoting lipid accumulation, hepatic inflammation, fibrosis, and cell death. Materials and methods: A review of chosen literature in the PubMed and Google Scholar databases was conducted, using the following key words: „Insulin resistane”, „Insulin resistance in obesity”, „Obesity”, „Insulin resistance NAFLD”, „Diebetes”, „Insulin resistance CVD” Summary: The consequences of insulin resistance are far-reaching. In the context of type 2 diabetes, it impedes glucose utilization by muscle cells, resulting in hyperglycemia and subsequent muscle cell damage, contributing to loss of mass and strength. Insulin resistance is also a central player in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), fostering lipid accumulation, hepatic inflammation, and, ultimately, fibrosis and cell death. Conclusions: In conclusion, understanding insulin resistance is paramount in addressing the rising prevalence of metabolic diseases globally Controlling insulin resistance emerges as a crucial aspect of managing these metabolic disorders and their complications. Further research into the mechanisms of IR formation and effective intervention strategies is imperative for improving public health outcomes.
Major causes of insuline resistance Ewa Lidia Krzewicka-Romaniuk; Dagna Agnieszka Siedlecka; Anna Pradiuch ...
Journal of education, health and sport,
09/2019, Volume:
9, Issue:
9
Journal Article
Peer reviewed
Open access
Causes of insulin resistance can be divided into innate and secondary. There are many reasons for insulin resistance, including genetic mutations like insulin receptor mutations, hormonal and ...pharmacological or immunological. However insulin resistance is most commonly associated with obesity. Obesity is associated with a low-grade inflammation of white adipose tissue (WAT) resulting from chronic activation of the innate immune system and which can subsequently lead to insulin resistance, impaired glucose tolerance and diabetes.
Major causes of insuline resistance Ewa Lidia Krzewicka-Romaniuk; Dagna Agnieszka Siedlecka; Anna Pradiuch ...
Journal of education, health and sport,
09/2019, Volume:
9, Issue:
9
Journal Article
Peer reviewed
Open access
Causes of insulin resistance can be divided into innate and secondary. There are many reasons for insulin resistance, including genetic mutations like insulin receptor mutations, hormonal and ...pharmacological or immunological. However insulin resistance is most commonly associated with obesity. Obesity is associated with a low-grade inflammation of white adipose tissue (WAT) resulting from chronic activation of the innate immune system and which can subsequently lead to insulin resistance, impaired glucose tolerance and diabetes.
Insulin plays a major neuroprotective and trophic function for cerebral cell population, thus countering apoptosis, beta-amyloid toxicity, and oxidative stress; favoring neuronal survival; and ...enhancing memory and learning processes. Insulin resistance and impaired cerebral glucose metabolism are invariantly reported in Alzheimer's disease (AD) and other neurodegenerative processes. AD is a fatal neurodegenerative disorder in which progressive glucose hypometabolism parallels to cognitive impairment. Although AD may appear and progress in virtue of multifactorial nosogenic ingredients, multiple interperpetuative and interconnected vicious circles appear to drive disease pathophysiology. The disease is primarily a metabolic/energetic disorder in which amyloid accumulation may appear as a by-product of more proximal events, especially in the late-onset form. As a bridge between AD and type 2 diabetes, activation of c-Jun N-terminal kinase (JNK) pathway with the ensued serine phosphorylation of the insulin response substrate (IRS)-1/2 may be at the crossroads of insulin resistance and its subsequent dysmetabolic consequences. Central insulin axis bankruptcy translates in neuronal vulnerability and demise. As a link in the chain of pathogenic vicious circles, mitochondrial dysfunction, oxidative stress, and peripheral/central immune-inflammation are increasingly advocated as major pathology drivers. Pharmacological interventions addressed to preserve insulin axis physiology, mitochondrial biogenesis-integral functionality, and mitophagy of diseased organelles may attenuate the adjacent spillover of free radicals that further perpetuate mitochondrial damages and catalyze inflammation. Central and/or peripheral inflammation may account for a local flood of proinflammatory cytokines that along with astrogliosis amplify insulin resistance, mitochondrial dysfunction, and oxidative stress. All these elements are endogenous stressor, pro-senescent factors that contribute to JNK activation. Taken together, these evidences incite to identify novel multi-mechanistic approaches to succeed in ameliorating this pandemic affliction.
Introduction
Patients with severe mental illness (SMI) have a higher risk of weight gain, dyslipidemia and insulin-resistance. It was observed that insulin resistance has a pathoplastic effect: in ...Schizophrenia it was associated with a greater severity of negative symptoms, whereas in Bipolar Disorder it was associated with more chronicity and rapid cycling. Moreover a correlation was observed between obesity and a worse outcome in Bipolar Disorder type I.
Objectives
We aimed at assessing the influence of dysmetabolisms on clinical characteristics in patients with SMI.
Methods
We recruited 78 patients with SMI consecutively hospitalized in the Psychiatry Clinic of the Ospedali Riuniti of Ancona, Italy. We administered a checklist for socio-demographic and clinical features (diagnosis, age of onset, illness duration, number of episodes, number of episodes per year, suicidal attempts and comorbidities), and evaluated the following metabolic parameters: weight, height, BMI, abdominal circumference, blood pressure, total cholesterol, HDL, triglycerides, glycemia and insulinemia. We determined insulin-resistance according to the HOMA-IR model. We performed bivariate Pearson correlations to compare metabolic and socio-demographic/clinical parameters.
Results
The analyses showed positive correlations between BMI and disease duration (P = 0.003), and BMI and the number of episodes (P = 0.022). Furthermore, a positive correlation was found between HOMA-IR and the number of episodes per year (P = 0.008). The associations remained statistically significant after controlling for age through partial correlations.
Conclusions
Weight gain and insulin-resistance in severe mental illness are associated with a more severe SMI, as suggested by the greater number of acute episodes.
Disclosure
No significant relationships.
Non-alcoholic fatty liver disease (NAFLD) is the most common form of chronic liver disease in the world. It is linked mainly to insulin resistance and metabolic syndrome including obesity and ...dyslipidemia. In addition, various endocrine dysfunctions including polycystic ovary syndrome (PCOS) and hypogonadism are involved in the development and progression of NAFLD. We need to know the disease pathophysiology more accurately due to the heterogeneity of clinical presentation of fatty liver disease. The liver is the major metabolic organ with sexual dimorphism. Sexual dimorphism is associated not only with behavioral differences between men and women, but also with physiological differences reflected in liver metabolism. In men, normal androgen levels prevent hepatic fat accumulation, whereas androgen deficiency induce hepatic steatosis. In women, higher androgens can increase the risk of NAFLD in PCOS. Sex hormone binding globulin (SHBG) is involved in androgen regulation. Recently, SHBG may be reported as a surrogate marker for NAFLD. Therefore, this review will focus on the mechanism of androgen dysfunction in the regulation of hepatic metabolism, the risk of developing NAFLD, and the potential role of SHBG in the course of NAFLD.; Keywords: Non-alcoholic fatty liver disease, insulin resistance, sexual dimorphism, androgen, sex hormone binding globulin.
Frozen shoulder is a common epidemiological affliction. Data acquired from people who suffer from this type of damage in other joints such as the hip, wrist and ankle also exist; although these ...syndromes are less common. Treatment for frozen shoulder is primarily physical (physiotherapy, manual therapy), secondary medical (corticosteroid injections) and finally surgical but with limited success. The difficulty in treating this type of condition successfully lies in the lack of knowledge about the risk factors involved and the pathophysiology underlying this mysterious syndrome. This review gives an overview of the current scientific position of frozen shoulder in terms of evolutionary factors, etiology, the different mechanisms of action involved, current treatment options and other possible interventions based on recent discoveries of pathophysiological mechanisms. The overall objective is to clarify several unknown aspects of a syndrome that affects up to 5% of the world's population.
Sex differences are defined as biology-linked differences between women and men that occur through the sex chromosomes and their effects on organ systems.
The objective of this prospective study was ...to determine risk factors for post-transplant diabetes mellitus (PTDM) in men and women.
A total of 417 patients (271 men and 146 women) were included in the monitored group. Age at the time of kidney transplantation (KT) >60 years and hypovitaminosis D at the time of KT (<20 μg/l) were identified as independent risk factors for PTDM in both men and women. It was further confirmed as an independent risk factor for men a waist circumference at the time of KT >94 cm, C-peptide at the time of KT >5 ng/ml, HOMA-IR >2 and triacylglycerols at the time of KT >1.7 mmol/l. In case of women, the dominant factor was BMI at the time of KT >30 kg/m2 and menopause at the time of KT. A significant decrease in C-peptide was recorded in women with PTDM.
It was confirmed that there are gender differences with regard to the development of PTDM after KT. Women show pancreas β cell dysfunction, whereas insulin resistance and metabolic syndrome are dominant in men.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The article presents research findings of reduced thyroid function impact on the background of insulin resistance on the specific links of metabolism, structure and function of the heart. It is found ...that in thyroid dysfunction, the main nosological form of myocardial lesion in female patients without concomitant cardiovascular disease is the development of metabolic endocrine cardiomyopathy. Feature of cardiac lesion is the absence of cardiosclerotic, myocardial and ischemic processes in hypothyroidism. Obscure clinical symptoms of the heart both in apparent and subclinical hypothyroidism are detected. Features of clinical, instrumental and laboratory changes in female patients with impaired thyroid function are a trend to systolic blood pressure increase, the absence of significant dyslipidemia, dysglycemia, and cardiocytolysis and hepatocytolysis. Thyroid hormone deficiency is associated with increased myocardial repolarization heterogeneity: subclinical hypothyroidism is accompanied by violation of repolarization processes and the development of electrical heterogeneity of ventricular myocardium, and in the apparent hypothyroidism changes are more linked with the violation of the homogeneity of the electrical impulse to the atria.
Aims
Ectopic fat is a recognized contributor to insulin resistance and metabolic dysfunction, while the role of fat deposition inside intestinal wall tissue remains understudied. We undertook this ...study to directly quantify and localize intramural fat deposition in duodenal tissue and determine its association with adiposity.
Methods
Duodenal tissues were collected from aged (21.2 ± 1.3 years, 19.5 ± 3.1 kg,
n
= 39) female baboons (
Papio
sp.). Fasted blood was collected for metabolic profiling and abdominal circumference (AC) measurements were taken. Primary tissue samples were collected at the major duodenal papilla at necropsy: one full cross section was processed for hematoxylin and eosin staining and evaluated; a second full cross section was processed for direct chemical lipid analysis on which percentage duodenal fat content was calculated.
Results
Duodenal fat content obtained by direct tissue quantification showed considerable variability (11.95 ± 6.93%) and was correlated with AC (
r
= 0.60,
p
< 0.001), weight (
r
= 0.38,
p
= 0.02), leptin (
r
= 0.63,
p
< 0.001), adiponectin (
r
= − 0.32,
p
< 0.05), and triglyceride (
r
= 0.41,
p
= 0.01). The relationship between duodenal fat content and leptin remained after adjusting for body weight and abdominal circumference. Intramural adipocytes were found in duodenal sections from all animals and were localized to the submucosa. Consistent with the variation in tissue fat content, the submucosal adipocytes were non-uniformly distributed in clusters of varying size. Duodenal adipocytes were larger in obese vs. lean animals (106.9 vs. 66.7 µm
2
,
p
= 0.02).
Conclusions
Fat accumulation inside the duodenal wall is strongly associated with adiposity and adiposity related circulating biomarkers in baboons. Duodenal tissue fat represents a novel and potentially metabolically active site of ectopic fat deposition.
Full text
Available for:
EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
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