scholarly journals Insulin Resistance and Alzheimer-like Reductions in Regional Cerebral Glucose Metabolism for Cognitively Normal Adults With Prediabetes or Early Type 2 Diabetes

2011 ◽  
Vol 68 (1) ◽  
Author(s):  
Laura D. Baker ◽  
Donna J. Cross ◽  
Satoshi Minoshima ◽  
Dana Belongia ◽  
G. Stennis Watson ◽  
...  
2021 ◽  
Vol 44 (3) ◽  
pp. 143-147
Author(s):  
Monira Hossain ◽  
Suraiya Begum ◽  
Shahana A Rahman

Introduction: Obesity in childhood is associated with many co-morbid conditions; one of them is alteration of glucose metabolism. Materials and Methods:This cross-sectional study was conducted among 100 overweight and obese children aged 5-16 years to determine the status of pre-diabetes (IFG and IGT) and type 2 diabetes mellitus (T2DM), attending the OPD, BSMMU, Dhaka. All overweight/obese children were included according to BMI for age and sex using CDC growth chart. Children taking steroid for any cause or having any endocrine disorder or syndrome was excluded from the study. Anthropometry and blood pressure measurement were done and skin manifestations of insulin resistance were looked for. Fasting lipid profile and oral glucose tolerance test (OGTT) was done for each child. Result: Among the studied children 62% were male and 38% female, 77% were obese and 23% were over weight. Evidence of insulin resistance were found among most of the children and most common evidence was dyslipidemia (80%) followed by acanthosis nigricans(76%). Skin manifestation of polycystic ovary syndrome (PCOS) was found in 3% of children. Impaired fasting glucose (IFG) was found in 4% and Impaired Glucose Tolerance (IGT) was found in 7% of children among them 4% had both IGT and IFT. No child was found diabetic in this study. Conclusion:Altered glucose metabolism was present in overweight and obese children of our children, so screening is recommended. Bangladesh J Child Health 2020; VOL 44 (3) :143-147


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Nils B. Jørgensen ◽  
Kirstine N. Bojsen-Møller ◽  
Carsten Dirksen ◽  
Christoffer Martinussen ◽  
Maria S. Svane ◽  
...  

Abstract To describe glucose metabolism in the late, weight stable phase after Roux-en-Y Gastric Bypass (RYGB) in patients with and without preoperative type 2 diabetes we invited 55 RYGB-operated persons from two existing cohorts to participate in a late follow-up study. 44 (24 with normal glucose tolerance (NGT)/20 with type 2 diabetes (T2D) before surgery) accepted the invitation (median follow-up 2.7 [Range 2.2–5.0 years]). Subjects were examined during an oral glucose stimulus and results compared to preoperative and 1-year (1 y) post RYGB results. Glucose tolerance, insulin resistance, beta-cell function and incretin hormone secretion were evaluated. 1 y weight loss was maintained late after surgery. Glycemic control, insulin resistance, beta-cell function and GLP-1 remained improved late after surgery in both groups. In NGT subjects, nadir glucose decreased 1 y after RYGB, but did not change further. In T2D patients, relative change in weight from 1 y to late after RYGB correlated with relative change in fasting glucose and HbA1c, whereas relative changes in glucose-stimulated insulin release correlated inversely with relative changes in postprandial glucose excursions. In NGT subjects, relative changes in postprandial nadir glucose correlated with changes in beta-cell glucose sensitivity. Thus, effects of RYGB on weight and glucose metabolism are maintained late after surgery in patients with and without preoperative T2D. Weight loss and improved beta-cell function both contribute to maintenance of long-term glycemic control in patients with type 2 diabetes, and increased glucose stimulated insulin secretion may contribute to postprandial hypoglycemia in NGT subjects.


2019 ◽  
Vol 111 (2) ◽  
pp. 448-458 ◽  
Author(s):  
Derrick Johnston Alperet ◽  
Salome Antonette Rebello ◽  
Eric Yin-Hao Khoo ◽  
Zoey Tay ◽  
Sharna Si-Ying Seah ◽  
...  

ABSTRACT Background In observational studies, coffee consumption has been consistently associated with a lower risk of type 2 diabetes mellitus. Trials examining the effect of coffee consumption on glucose metabolism have been limited by the use of surrogate insulin sensitivity indices, small sample sizes, lack of blinding, and short follow-up duration. Objectives We aimed to overcome limitations of previously conducted coffee trials in a randomized placebo-controlled trial of the effect of coffee consumption on insulin sensitivity. Methods We conducted a 24-wk randomized placebo-controlled trial in 126 overweight, non–insulin sensitive (HOMA-IR ≥1.30), Chinese, Malay, and Asian-Indian males and females aged 35–69 y. Participants were randomly assigned to receive 4 cups of instant regular coffee (n = 62) or 4 cups of a coffee-like placebo beverage (n = 64) per day. The primary outcome was the amount of glucose metabolized per kilogram of body weight per minute (Mbw) assessed during steady-state conditions with a hyperinsulinemic euglycemic clamp. Secondary outcomes included other clamp-based insulin sensitivity measures, biological mediators of insulin sensitivity, and measures of fasting glucose metabolism. Results Coffee consumption did not significantly change insulin sensitivity compared with placebo (percentage mean difference in Mbw = 4.0%; 95% CI: −8.3, 18.0%; P = 0.53). Furthermore, no significant differences in fasting plasma glucose (2.9%; 95% CI: −0.4, 6.3%; P = 0.09) or biological mediators of insulin resistance, such as plasma adiponectin (2.3%; 95% CI: −1.4, 6.2%; P = 0.22), were observed between coffee and placebo groups over 24 wk of intervention. Participants in the coffee arm experienced a loss of fat mass (FM) (−3.7%; 95% CI: −6.3, −1.1%; P = 0.006) and reduction in urinary creatinine concentrations (−21.2%; 95% CI: −31.4, −9.5%; P = 0.001) compared with participants in the placebo arm over 24 wk of intervention. Conclusions Consuming 4 cups/d of caffeinated coffee for 24 wk had no significant effect on insulin sensitivity or biological mediators of insulin resistance but was associated with a modest loss of FM and reduction in urinary creatinine concentrations. This trial was registered at clinicaltrials.gov as NCT01738399. Registered on November 28, 2012. Trial sponsor: Nestlé Research, Lausanne, Switzerland. Trial site: National University of Singapore.


Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2636 ◽  
Author(s):  
Leslie A. Consitt ◽  
Courtney Dudley ◽  
Gunjan Saxena

Aging is associated with insulin resistance and the development of type 2 diabetes. While this process is multifaceted, age-related changes to skeletal muscle are expected to contribute to impaired glucose metabolism. Some of these changes include sarcopenia, impaired insulin signaling, and imbalances in glucose utilization. Endurance and resistance exercise training have been endorsed as interventions to improve glucose tolerance and whole-body insulin sensitivity in the elderly. While both types of exercise generally increase insulin sensitivity in older adults, the metabolic pathways through which this occurs can differ and can be dependent on preexisting conditions including obesity and type 2 diabetes. In this review, we will first highlight age-related changes to skeletal muscle which can contribute to insulin resistance, followed by a comparison of endurance and resistance training adaptations to insulin-stimulated glucose metabolism in older adults.


2016 ◽  
Vol 36 (23) ◽  
pp. 2956-2966 ◽  
Author(s):  
Sezin Dagdeviren ◽  
Dae Young Jung ◽  
Eunjung Lee ◽  
Randall H. Friedline ◽  
Hye Lim Noh ◽  
...  

Skeletal muscle insulin resistance is a major characteristic of obesity and type 2 diabetes. Although obesity-mediated inflammation is causally associated with insulin resistance, the underlying mechanism is unclear. Here, we examined the effects of chronic obesity in mice with muscle-specific overexpression of interleukin-10 (M IL10 ). After 16 weeks of a high-fat diet (HFD), M IL10 mice became markedly obese but showed improved insulin action compared to that of wild-type mice, which was largely due to increased glucose metabolism and reduced inflammation in skeletal muscle. Since leptin regulates inflammation, the beneficial effects of interleukin-10 (IL-10) were further examined in leptin-deficient ob / ob mice. Muscle-specific overexpression of IL-10 in ob / ob mice (MCK-IL10 ob / ob ) did not affect spontaneous obesity, but MCK-IL10 ob / ob mice showed increased glucose turnover compared to that in ob / ob mice. Last, mice with muscle-specific ablation of IL-10 receptor (M-IL10R −/− ) were generated to determine whether IL-10 signaling in skeletal muscle is involved in IL-10 effects on glucose metabolism. After an HFD, M-IL10R −/− mice developed insulin resistance with reduced glucose metabolism compared to that in wild-type mice. Overall, these results demonstrate IL-10 effects to attenuate obesity-mediated inflammation and improve insulin sensitivity in skeletal muscle, and our findings implicate a potential therapeutic role of anti-inflammatory cytokines in treating insulin resistance and type 2 diabetes.


2021 ◽  
Vol 18 (5) ◽  
pp. 995-999
Author(s):  
Yufang Liu ◽  
Fang Wang ◽  
Xiue Xu ◽  
Hui Cong ◽  
Guiyan Chen

Purpose: To study the effects of angiotensin-(1-7) (angiot (1-7) intervention on angiotensin converting enzyme (ACE)-angiot-(1-7)-Mas pathway, hepatic glucose metabolism, and insulin resistance in rats with type 2 diabetes. Methods: Thirty-six Sprague Dawley rats were randomly divided into normal control, diabetic control and study groups (12 rats per group). Rats in the normal group were fed normal feed, while rats in the observation and diabetic control groups were type-2 diabetes model, and were given subcutaneous injection of angiot-(1-7) for 8 weeks. Serum insulin resistance index (IRI) and fasting insulin (FINS) were assayed. Other parameters measured were the levels of ACE2 and Mas receptor mRNA in liver tissues. Results: The levels of FINS in the study and control groups decreased, relative to normal control, while the levels of IRI was elevated (p < 0.05). There were significant increases in study group levels of Mas and ACE2, while angiot-(1-7) was lower, relative to control group (p < 0.05). The expressions of ACE2 and Mas receptors in study and diabetic control rats groups were downregulated, when compared to normal control. The expressions of ACE2 and Mas receptors also decreased in the study group exposed to angiot-(1-7) (p < 0.05). Conclusion: Angiot-(1-7) significantly increases the levels of FINS and IR, improves hepatic glucose metabolism and enhances ACE2-angiot-(1-7)-Mas pathway. Thus, angiot-(1-7) may be a new drug candidate for the treatment of type 2 diabetes.


2011 ◽  
Vol 81 (5) ◽  
pp. 317-327 ◽  
Author(s):  
Moira S. Hutchinson ◽  
Yngve Figenschau ◽  
Bjørg Almås ◽  
Inger Njølstad ◽  
Rolf Jorde

The relationships between vitamin D concentrations, hyperglycemia, and insulin resistance remain uncertain. During 2008 - 2010, an oral glucose tolerance test was performed in 3520 subjects from Tromsø, Norway. Serum 25-hydroxyvitamin D [25(OH)D] was measured in 1193 subjects with normal glucose tolerance, in 304 with isolated impaired fasting glucose, in 254 with isolated impaired glucose tolerance, in 139 with a combination of the two, and in 194 subjects with type 2 diabetes. Serum 25(OH)D did not differ between subjects with isolated impaired fasting glucose or impaired glucose tolerance, but was lower in all groups of deranged glucose metabolism as compared with normal subjects. These differences could not be explained by differences in intakes of vitamin D from cod liver oil or other supplements and remained statistically significant after adjustment for gender, age, body mass index, physical activity score, and month of examination. When the cohort was divided according to serum 25(OH)D quartiles, there was an improvement in all measures of glucose metabolism (fasting and 2-hour plasma glucose, serum insulin, HbA1c) and estimates of insulin resistance (QUICKI , HOMA-IR, ISI0.120) with increasing serum 25(OH)D quartile. However, interventional studies are needed to prove a causal relationship between vitamin D and glucose metabolism.


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