• Title/Summary/Keyword: Insulin Resistance

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Prediction of Type 2 Diabetes Remission after Bariatric or Metabolic Surgery

  • Park, Ji Yeon
    • Journal of Obesity & Metabolic Syndrome
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    • v.27 no.4
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    • pp.213-222
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    • 2018
  • Bariatric surgery has evolved from a surgical measure for treating morbid obesity to an epochal remedy for treating metabolic syndrome as a whole, which is represented by type 2 diabetes mellitus. Numerous clinical trials have advocated bariatric or metabolic surgery over nonsurgical interventions because of markedly superior metabolic outcomes in morbidly obese patients who satisfy traditional criteria for bariatric surgery (body mass index [BMI] >$35kg/m^2$) and in less obese or simply overweight patients. Nevertheless, not all diabetes patients achieve the most desirable outcomes; i.e., diabetes remission after metabolic surgery. Thus, candidates for metabolic surgery should be carefully selected based on comprehensive preoperative assessments of the risk-benefit ratio. Predictors for diabetes remission after metabolic surgery may be classified into two groups based on mechanism of action. The first is indices for preserved pancreatic beta-cell function, including younger age, shorter duration of diabetes, and higher C-peptide level. The second is the potential for an insulin resistance reduction, including higher baseline BMI and visceral fat area. Several prediction models for diabetes remission have been suggested by merging these two to guide the joint decision-making process between clinicians and patients. Three such models, DiaRem, ABCD, and individualized metabolic surgery scores, provide an intuitive scoring system and have been validated in an independent external cohort and can be utilized in routine clinical practice. These prediction models need further validation in various ethnicities to ensure universal applicability.

Vitamin C Inhibits Visceral Adipocyte Hypertrophy and Lowers Blood Glucose Levels in High-Fat-Diet-Induced Obese C57BL/6J Mice

  • Park, Younghyun;Jang, Joonseong;Lee, Dongju;Yoon, Michung
    • Biomedical Science Letters
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    • v.24 no.4
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    • pp.311-318
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    • 2018
  • Vitamin C (ascorbic acid) supplementation has been suggested to negatively correlate with obesity in humans and other animals. Previous studies, including ours, have demonstrated that a high-fat diet (HFD) induces obesity and related diseases such as hyperlipidemia, hyperglycemia, insulin resistance, and nonalcoholic fatty liver disease. Here, we investigated the effects of vitamin C on visceral adipocyte hypertrophy and glucose intolerance in C57BL/6J mice. Mice received a low-fat diet (LFD, 10% kcal fat), HFD (45% kcal fat), or the same HFD supplemented with vitamin C (HFD-VC, 1% w/w) for 15 weeks. Visceral adiposity and glucose intolerance were examined using metabolic measurements, histology, and gene expression analyses. Mice in the HFD-VC supplementation group had reduced body weight, mesenteric fat mass, and mesenteric adipocyte size compared with HFD-fed mice. Vitamin C intake in obese mice also decreased the mRNA levels of lipogenesis-related genes (i.e., stearoyl-CoA desaturase 1 and sterol regulatory element-binding protein 1c) in mesenteric adipose tissues, inhibited hyperglycemia, and improved glucose tolerance. In addition, vitamin C attenuated the HFD-induced increase in the size of pancreatic islets. These results suggest that vitamin C suppresses HFD-induced visceral adipocyte hypertrophy and glucose intolerance in part by decreasing the visceral adipose expression of genes involved in lipogenesis.

Pharmacologic therapy for nonalcoholic steatohepatitis focusing on pathophysiology

  • Yoon, In Cheol;Eun, Jong Ryeol
    • Journal of Yeungnam Medical Science
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    • v.36 no.2
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    • pp.67-77
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    • 2019
  • The paradigm of chronic liver diseases has been shifting. Although hepatitis B and C viral infections are still the main causes of liver cirrhosis and hepatocellular carcinoma (HCC), the introduction of effective antiviral drugs may control or cure them in the near future. In contrast, the burden of nonalcoholic fatty liver disease (NAFLD) has been increasing for decades, and 25 to 30% of the general population in Korea is estimated to have NAFLD. Over 10% of NAFLD patients may have nonalcoholic steatohepatitis (NASH), a severe form of NAFLD. NASH can progress to cirrhosis and HCC. NASH is currently the second leading cause to be placed on the liver transplantation list in the United States. NAFLD is associated with obesity, type 2 diabetes, dyslipidemia, and metabolic syndrome. The pathophysiology is complex and associated with lipotoxicity, inflammatory cytokines, apoptosis, and insulin resistance. The only proven effective treatment is weight reduction by diet and exercise. However, this may not be effective for advanced fibrosis or cirrhosis. Therefore, effective drugs are urgently needed for treating these conditions. Unfortunately, no drugs have been approved for the treatment of NASH. Many pharmaceutical companies are trying to develop new drugs for the treatment of NASH. Some of them are in phase 2 or 3 clinical trials. Here, pharmacologic therapies in clinical trials, as well as the basic principles of drug therapy, will be reviewed, focusing on pathophysiology.

Concurrent SHORT syndrome and 3q duplication syndrome

  • Boaz, Alexander M.;Grasso, Salvatore A.;DeRogatis, Michael J.;Beesley, Ellis N.
    • Journal of Genetic Medicine
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    • v.16 no.1
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    • pp.15-18
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    • 2019
  • SHORT syndrome is an extremely rare congenital condition due to a chromosomal mutation of the PIK3R1 gene found at 5q13.1. SHORT is a mnemonic representing six manifestations of the syndrome: (S) short stature, (H) hyperextensibility of joints and/or inguinal hernia, (O) ocular depression, (R) Rieger anomaly, and (T) teething delay. Other key aspects of this syndrome not found in the mnemonic include lipodystrophy, triangular face with dimpled chin (progeroid facies, commonly referred to as facial gestalt), hearing loss, vision loss, insulin resistance, and intrauterine growth restriction (IUGR). 3q duplication syndrome is rare syndrome that occurs due to a gain of function mutation found at 3q25.31-33 that presents with a wide array of manifestations including internal organ defects, genitourinary malformations, hand and foot deformities, and mental disability. We present a case of a 2 year and 3 month old male with SHORT syndrome and concurrent 3q duplication syndrome. The patient presented at birth with many of the common manifestations of SHORT syndrome such as bossing of frontal bone of skull, triangular shaped face, lipodystrophy, micrognathia, sunken eyes, and thin, wrinkled skin (progeroid appearance). Additionally, he presented with findings associated with 3q duplication syndrome such as cleft palate and cryptorchidism. Although there is no specific treatment for these conditions, pediatricians should focus on referring patients to various specialists in order to treat each individual manifestation.

Emerging roles of PHLPP phosphatases in metabolism

  • Cha, Jong-Ho;Jeong, Yelin;Oh, Ah-Reum;Lee, Sang Bae;Hong, Soon-Sun;Kim, KyeongJin
    • BMB Reports
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    • v.54 no.9
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    • pp.451-457
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    • 2021
  • Over the last decades, research has focused on the role of pleckstrin homology (PH) domain leucine-rich repeat protein phosphatases (PHLPPs) in regulating cellular signaling via PI3K/Akt inhibition. The PKB/Akt signaling imbalances are associated with a variety of illnesses, including various types of cancer, inflammatory response, insulin resistance, and diabetes, demonstrating the relevance of PHLPPs in the prevention of diseases. Furthermore, identification of novel substrates of PHLPPs unveils their role as a critical mediator in various cellular processes. Recently, researchers have explored the increasing complexity of signaling networks involving PHLPPs whereby relevant information of PHLPPs in metabolic diseases was obtained. In this review, we discuss the current knowledge of PHLPPs on the well-known substrates and metabolic regulation, especially in liver, pancreatic beta cell, adipose tissue, and skeletal muscle in relation with the stated diseases. Understanding the context-dependent functions of PHLPPs can lead to a promising treatment strategy for several kinds of metabolic diseases.

Effect of Sharbat Afsantīn in Poly Cystic Ovarian Disease - An Open Observational Study

  • Zubair, Zainab;Shameem, Ismath;Begum, Wajeeha
    • CELLMED
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    • v.12 no.3
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    • pp.10.1-10.12
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    • 2022
  • Objective: The objective of the study was to evaluate the effect of Sharbat Afsantin in Polycystic Ovarian Disease. Methods: An open observational study was carried out in the Department of Ilmul Qabalat wa Amraze Niswan. Diagnosed cases(n=30) of PCOD were included in the study. Patients with thyroid dysfunction, systemic diseases, on hormonal treatment in last three months, pregnancy and lactation were excluded. Research drug (Sharbat Afsantin) was administered orally in a dose of 25ml twice daily for 15 days/cycle for three consecutive cycles. Outcome measures were, changes in subjective parameters (duration of cycle, duration and amount of flow and weight reduction) and objective parameters {pictorial blood loss assessment chart (PBAC) score, basal metabolic index (BMI), modified Ferriman Gallwey (mFG) score, acanthosis nigricans scale and pelvic ultrasonography}. Data were analyzed using paired Student 't' test. Results: Changes in duration of cycle, duration and amount of flow were achieved in 83.3%, 50% and 40% patients respectively and weight reduction in 30% patients. Changes in PBAC score and BMI were achieved in 50% and 30% patients respectively and 30% patients showed normal findings on pelvic ultrasonography. Conclusion: Sharbat Afsantin can be used as an alternate remedy in PCOD patients, as it has significant effect to regularize menstruation by reduction in BMI and probably by improving insulin resistance in PCOD. No adverse effect of Sharbat Afsantin was noted during the trial.

The Effect of Atypical Anti-psychotic Agents on Obesity and Glucose Metabolism (비정형 항정신병약제가 비만과 당대사에 미치는 영향)

  • Sang Ah Lee;Suk Ju Cho;Jae Cheol Moon
    • Journal of Medicine and Life Science
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    • v.18 no.3
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    • pp.49-55
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    • 2021
  • Atypical antipsychotics are more effective than typical antipsychotics and have fewer side effects such as tardive dyskinesia and extrapyramidal symptoms; therefore, prescriptions of atypical antipsychotics are increasing. However, recently, it has been reported that atypical antipsychotics have a higher incidence of diabetes, hyperglycemia, and obesity than typical antipsychotics. Atypical antipsychotics induce obesity-inhibiting appetite-related receptors such as serotonin and dopamine. Decreased exercise due to improving psychotic symptoms, and genetic characterictics can also cause weight gain. Hyperglycemia and hypoglycemia were another metabolic problem related to treatment with atypical antipsychotics. The mechanisms of hyperglycemia were mainly related obesity, decreased anorexigenic hormones, and increased insulin resistance in multiple organs. There are also reports that genes related to diabetes have an effect on the incidence of diabetes mellitus treated with atypical antipsychotics. On the other hand, although it is not clear why hypoglycemia occurs, it documented in case reports all over the world. There are more reports of atypical antipsychotics than typical antipsychotics and these are frequently reported in Asians. Further research on the mechanism of hypoglycemia related to atypical antipsychotics is strongly recommended.

A Clinical Report on a Patient with Type 2 Diabetes

  • Shin, Ae-sook;Gwak, Ja-young;Cho, Seung-yeon;Lee, In-whan;Kim, Hye-mi;Kim, Na-hee;Park, Sung-wook;Park, Jung-mi;Ko, Chang-nam;Bae, Hyung-sup
    • The Journal of the Society of Stroke on Korean Medicine
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    • v.10 no.1
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    • pp.68-73
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    • 2009
  • Type 2 diabetes mellitus (T2DM) is a progressive disorder caused by a combination of insulin resistance and 𝛽 cell dysfunction. Sogal(消渴) is a traditional Korean medical term referring to a condition pertaining 3 major symptoms - thirst, polyphasia, polyuria. Sogal has been reported to have similar characteristics with DM. This case report demonstrates a patient with T2DM complaining of typical Sogal symptoms. We diagnosed him as So-yang person Sogal and treated him with acupuncture and herbal medicine.

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Effects of treadmill exercise on the regulatory mechanisms of mitochondrial dynamics and oxidative stress in the brains of high-fat diet fed rats

  • Koo, Jung-Hoon;Kang, Eun-Bum
    • Korean Journal of Exercise Nutrition
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    • v.23 no.1
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    • pp.28-35
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    • 2019
  • [Purpose] The purpose of this study was to investigate the effects of treadmill exercise on oxidative stress in the hippocampal tissue and mitochondrial dynamic-related proteins in rats fed a long-term high-fat diet (HFD). [Methods] Obesity was induced in experimental animals using high fat feed, and the experimental groups were divided into a normal diet-control (ND-CON; n=12), a high fat diet-control (HFD-CON; n=12) and a high fat diet-treadmill exercise (HFD-TE; n=12) group. The rats were subsequently subjected to treadmill exercise (progressively increasing load intensity) for 8 weeks (5 min at 8 m/min, then 5 min at 11 m/min, and finally 20 min at 14 m/min). We assessed weight, triglyceride (TG) concentration, total cholesterol (TC), area under the curve, homeostatic model assessment of insulin resistance, and AVF/body weight. Western blotting was used to examine expression of proteins related to oxidative stress and mitochondrial dynamics, and immunohistochemistry was performed to examine the immunoreactivity of gp91phox. [Results] Treadmill exercise effectively improved the oxidative stress in the hippocampal tissue, expression of mitochondrial dynamic-related proteins, and activation of NADPH oxidase (gp91phox) and induced weight, blood profile, and abdominal fat loss. [Conclusion] Twenty weeks of high fat diet induced obesity, which was shown to inhibit normal mitochondria fusion and fission functions in hippocampal tissues. However, treadmill exercise was shown to have positive effects on these pathophysiological phenomena. Therefore, treadmill exercise should be considered during prevention and treatment of obesity-induced metabolic diseases.

Menopausal Hormone Therapy for Preventing Weight Gain and Cardiovascular Disease (체중과 심혈관 질환에 대한 폐경기 호르몬 요법의 효과)

  • Yeong Sook Yoon
    • Archives of Obesity and Metabolism
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    • v.2 no.2
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    • pp.54-63
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    • 2023
  • Estrogen is crucial in regulating food intake, energy expenditure, glucose metabolism, and lipid metabolism. During menopause, the decline in estrogen levels predisposes women to weight gain, abdominal obesity, insulin resistance, type 2 diabetes, hypertension, and cardiovascular disease (CVD). Menopausal hormone therapy (MHT) prevents weight gain, improves lipid metabolism by lowering low-density lipoprotein cholesterol while raising high-density lipoprotein cholesterol, and delays the onset of type 2 diabetes in menopausal women. The effect of MHT on CVD in menopausal women remains controversial. The Women's Health Initiative study was terminated prematurely after it revealed that hormone administration increased the risk of myocardial infarction, stroke, and thromboembolism. However, some studies have found that MHT had no effect or decreased the risk of CVD. The inconsistent results were likely due to multiple factors, including the timing of hormone therapy initiation, duration of therapy, type and dosage, and presence or absence of CVD risk factors at the start of treatment. Despite its benefits in terms of managing weight gain and reducing the risk of type 2 diabetes, dyslipidemia, and CVD associated with obesity, it is not recommended as the primary therapy for weight loss or diabetes prevention. MHT is primarily indicated for postmenopausal women, who are likely to benefit from its potential to prevent weight gain and improve lipid metabolism.