scholarly journals Morphological and functional adaptation of pancreatic islet blood vessels to insulin resistance is impaired in diabetic db/db mice

2022 ◽  
pp. 166339
Author(s):  
Yuka Okajima ◽  
Takashi Matsuzaka ◽  
Shun Miyazaki ◽  
Kaori Motomura ◽  
Hiroshi Ohno ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Vessels ◽  
Pancreatic Islet ◽  
Functional Adaptation

Electroacupuncture Mitigates Endothelial Dysfunction via Effects on the Pi3K/Akt Signalling Pathway in High Fat Diet-Induced Insulin-Resistant Rats

2018 ◽  
Vol 36 (3) ◽  
pp. 162-169 ◽  
Author(s):  
Danchun Lan ◽  
Nenggui Xu ◽  
Jian Sun ◽  
Zhixing Li ◽  
Rongzhen Liao ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Pancreatic Islet ◽  
High Fat Diet ◽  
Negative Impact ◽  
Fasting Blood Glucose ◽  
Signalling Pathway ◽  
Control Group ◽  
Model Assessment ◽  
High Fat

Objective To investigate the effect of electroacupuncture (EA) on endothelial dysfunction related to high fat diet (HFD)-induced insulin resistance through the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) signalling pathway. Methods Twenty-four male Sprague-Dawley rats were fed a regular diet (Control group, n=8) or a HFD (n=16) for 12 weeks to induce an insulin resistance model. HFD-fed rats were divided into two groups that remained untreated (HFD group, n=8) or received electroacupuncture (HFD+EA group, n=8). EA was applied at PC6, ST36, SP6 and BL23. At the end of the experiment, fasting blood glucose (FBG), serum insulin (FINS), serum C-peptide (C-P) and homeostatic model assessment of insulin resistance (HOMA-IR) indices were determined. Pancreatic islet samples were subjected to histopathological examination. The thoracic aorta was immunostained with anti-rat insulin receptor substrate (IRS)-1, Akt and endothelial nitric oxide synthase (eNOS) antibodies. mRNA and protein expression of IRS-1, PI3K, Akt2 and eNOS in the vascular endothelium were determined by real-time PCR and Western blot analysis, respectively. Results The bodyweight increase of the HFD+EA group was smaller than that of the untreated HFD group. Compared with the HFD group, the levels of FBG, FINS, C-P and HOMA-IR in the HFD+EA group decreased significantly (P<0.01). Histopathological evaluation indicated that EA improved pancreatic islet inflammation. The expression of endothelial markers, such as IRS-1, PI3K, Akt2 and eNOS, decreased in the HFD group, while EA treatment appeared to ameliorate the negative impact of diet. Conclusion EA may improve insulin resistance and attenuate endothelial dysfunction, and therefore could play a potential role in the prevention or treatment of diabetic complications and cardiovascular disease through the PI3K/Akt signalling pathway.

scholarly journals Five stages of progressive β-cell dysfunction in the laboratory Nile rat model of type 2 diabetes

2016 ◽  
Vol 229 (3) ◽  
pp. 343-356 ◽  
Author(s):  
Kaiyuan Yang ◽  
Jonathan Gotzmann ◽  
Sharee Kuny ◽  
Hui Huang ◽  
Yves Sauvé ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Cell Mass ◽  
Β Cell ◽  
High Fiber ◽  
Insulin Resistant ◽  
Cell Dysfunction

We compared the evolution of insulin resistance, hyperglycemia, and pancreatic β-cell dysfunction in the Nile rat (Arvicanthis niloticus), a diurnal rodent model of spontaneous type 2 diabetes (T2D), when maintained on regular laboratory chow versus a high-fiber diet. Chow-fed Nile rats already displayed symptoms characteristic of insulin resistance at 2 months (increased fat/lean mass ratio and hyperinsulinemia). Hyperglycemia was first detected at 6 months, with increased incidence at 12 months. By this age, pancreatic islet structure was disrupted (increased α-cell area), insulin secretion was impaired (reduced insulin secretion and content) in isolated islets, insulin processing was compromised (accumulation of proinsulin and C-peptide inside islets), and endoplasmic reticulum (ER) chaperone protein ERp44 was upregulated in insulin-producing β-cells. By contrast, high-fiber-fed Nile rats had normoglycemia with compensatory increase in β-cell mass resulting in maintained pancreatic function. Fasting glucose levels were predicted by the α/β-cell ratios. Our results show that Nile rats fed chow recapitulate the five stages of progression of T2D as occurs in human disease, including insulin-resistant hyperglycemia and pancreatic islet β-cell dysfunction associated with ER stress. Modification of diet alone permits long-term β-cell compensation and prevents T2D.

scholarly journals Perivascular Adipose Tissue and Cardiometabolic Disease

2013 ◽  
Vol 5 (1) ◽  
pp. 13
Author(s):  
Anna Meiliana ◽  
Andi Wijaya
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Blood Vessels ◽  
Vascular Function ◽  
Immune Cell ◽  
The Body ◽  
Cardiometabolic Disease ◽  
Perivascular Adipose Tissue ◽  
Nitric Oxide Signaling ◽  
Fat Depots

BACKGROUND: Obesity is associated with insulin resistance, hypertension, and cardiovascular disease, but the mechanisms underlying these associations are incompletely understood. Microvascular dysfunction may play an important role in the pathogenesis of both insulin resistance and hypertension in obesity.CONTENT: Perivascular adipose tissue (PVAT) is a local deposit of adipose tissue surrounding the vasculature. PVAT is present throughout the body and has been shown to have a local effect on blood vessels. The influence of PVAT on the vasculature changes with increasing adiposity. PVAT similarly to other fat depots, is metabolically active, secreting a wide array of bioactive substances, termed ‘adipokines’. Adipokines include cytokines, chemokines and hormones that can act in a paracrine, autocrine or endocrine fashion. Many of the proinflammatory adipokines upregulated in obesity are known to influence vascular function, including endothelial function, oxidative stress, vascular stiffness and smooth muscle migration. Adipokines also stimulate immune cell migration into the vascular wall, potentially contributing to the inflammation found in atherosclerosis. Finally, adipokines modulate the effect of insulin on the vasculature, thereby decreasing insulin-mediated muscle glucose uptake. This leads to alterations in nitric oxide signaling, insulin resistance and potentially atherogenesis.SUMMARY: PVAT surrounds blood vessels. PVAT and the adventitial layer of blood vessels are in direct contact with each other. Healthy PVAT secretes adipokines and regulates vascular function. Obesity is associated with changes in adipokine secretion and the resultant inflammation of PVAT. The dysregulation of adipokines changes the effect of PVAT on the vasculature. Changes in perivascular adipokines secretion in obesity appear to contribute to the development of obesity-mediated vascular disease.KEYWORDS: obesity, perivascular adipose tissue, PVAT, cardiometabolic disease, adipokine

Peroxidative stress in diabetic blood vessels. Reversal by pancreatic islet transplantation

Diabetes ◽  
1995 ◽  
Vol 44 (8) ◽  
pp. 884-889 ◽  
Author(s):  
G. M. Pieper ◽  
M. Jordan ◽  
L. A. Dondlinger ◽  
M. B. Adams ◽  
A. M. Roza
Keyword(s):  
Blood Vessels ◽  
Islet Transplantation ◽  
Pancreatic Islet ◽  
Pancreatic Islet Transplantation ◽  
Peroxidative Stress

Peroxidative Stress in Diabetic Blood Vessels: Reversal by Pancreatic Islet Transplantation

Diabetes ◽  
1995 ◽  
Vol 44 (8) ◽  
pp. 884-889 ◽  
Author(s):  
G. M. Pieper ◽  
M. Jordan ◽  
L. A. Dondlinger ◽  
M. B. Adams ◽  
A. M. Roza
Keyword(s):  
Blood Vessels ◽  
Islet Transplantation ◽  
Pancreatic Islet ◽  
Pancreatic Islet Transplantation ◽  
Peroxidative Stress

Age-dependent onset of liver-specific IGF-I gene deficiency and its persistence in old age: implications for postnatal growth and insulin resistance in LID mice

2005 ◽  
Vol 289 (2) ◽  
pp. E288-E295 ◽  
Author(s):  
Zhengyi Tang ◽  
Rong Yu ◽  
Yarong Lu ◽  
A. F. Parlow ◽  
Jun-Li Liu
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Old Age ◽  
Pancreatic Islet ◽  
Postnatal Growth ◽  
Gene Deficiency ◽  
Igf I ◽  
Age Dependent ◽  
I Gene

To explore the limitations of the liver-specific IGF-I gene-deficient (LID) model and to further evaluate the role of endocrine IGF-I in early postnatal life and old age, we have studied these mice during the prepubertal period (from birth to 3 wk of age) and when they are 2 yr old. During the first 2 wk of life, IGF-I gene deficiency and the resulting reduction in serum IGF-I levels in LID mice did not reach sufficiently low levels when mice experience the most rapid and growth hormone (GH)-independent growth. It suggests that the role of liver-derived IGF-I in prepubertal, GH-independent postnatal growth cannot be established. From our previous studies, liver IGF-I mRNA level was abolished in adult LID mice, which causes elevated GH level, insulin resistance, pancreatic islet enlargement, and hyperinsulinemia. Interestingly in 2-yr-old LID mice, although liver IGF-I mRNA and serum IGF-I levels were still suppressed, serum insulin and GH levels had returned to normal. Compared with same-sex control littermates, aged male LID mice had significantly reduced body weight and fat mass and exhibited normal insulin sensitivity. On the other hand, aged female LID mice exhibited normal weight and marginal resistance to insulin actions. The pancreatic islet percentage (reflecting islet cell mass) was also restored to normal levels in aged LID mice. Thus, although the IGF-I gene deficiency is well maintained into old age, the insulin sensitivity, islet enlargement, and hyperinsulinemia that occurred in young adult mice have been mostly restored to normal levels, further supporting the age-dependent and sexual dimorphic features of the LID mice.

scholarly journals Beneficial effects of liraglutide on peripheral blood vessels

2020 ◽  
pp. 89-89
Author(s):  
Xueyang Zhang ◽  
Yongbo Wang ◽  
Simengge Yang ◽  
Junwei Zong ◽  
Xuejiao Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Blood Vessels ◽  
Peripheral Blood ◽  
Cell Function ◽  
Hypoglycemic Effect ◽  
Postprandial Blood Glucose ◽  
Diabetic Patients ◽  
Model Assessment

Background/Aim. Macroangiopathy is the major cause of death and disability in type 2 diabetic patients. Studies have shown that liraglutide, a GLP-1 receptor agonist, can protect the cardiovascular system by inhibiting chronic inflammation of diabetes. However, the effects of liraglutide on peripheral blood vessels and peripheral blood leukocytes have not reported at home and abroad. Objective: To observe and explore vascular protection and mechanism of liraglutide in addition to hypoglycemic effect. Methods: 60 hospitalized patients with type 2 diabetes were recruited from December 2013 to December 2014 at the First Affiliated Hospital of Dalian Medical University. Before the treatment of liraglutide?height and weight were measure to calculate body mass index (BMI). Blood urea nitrogen (BUN) and so on were detected. Homeostasis model assessment of insulin resistance (HOMA-IR) and islet ? cell function (HOMA-?) were computed. After applying liraglutide for three months, all indexes were measured again. The effects of liraglutide on these indexes were analyzed by paired sample t test. Results: After treatment with liraglutide, HbA1c (8.46?1.62 vs 7.26?1.40%) and 2hPBG (11.95 vs 9.6 mmol/L) decreased significantly (P<0.05). Body weight (87.3 vs 82.5 kg) and BMI (30.37 vs 28.63 kg/m2) decreased by 5.5% and 5.7% (P<0.05). TG?2.57?1.54 vs 1.81?0.70 mmol/L? and LDL-C?2.92?0.78 vs 1.89?0.66 mmol/L?reduced significantly (P<0.05). ABI decreased from 1.24?0.10 to 1.14?0.06 cm/s by 8%, while baPWV decreased from 1442.15?196.26 to 1316.85?146.63 cm/s by 8.7%, and both difference was statistically significant (P < 0.001). Conclusion: Liraglutide, with a good hypoglycemic effect, can significantly reduce postprandial blood glucose and HbA1c, but can not significantly improve fasting plasma glucose, insulin resistance and islet function. It also significantly decreased body weight, BMI and TG. Liraglutide can significantly lower ba-PWV and ABI to protect peripheral blood vessels.

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