Hyperglycemic hemianopia as a stroke mimic in hyperosmolar non ketotic state in type 2 Diabetes

1970 ◽  
Vol 1 (1) ◽  
pp. 7-9
Author(s):  
Sumesh Raj ◽  
Manoj Parameswaran ◽  
Jijun M Ignatius

Stroke mimics are differential presentations of various systemic disorders that simulate an acute stroke. The conditions vary from numerous metabolic and psychiatric conditions to central nervous system involvement in the form of cerebral tumours, complicated migraine, myasthenia gravis and multiple sclerosis. Metabolic disorders represent a small mimicking subgroup of acute focal neurological deficits. They include hypoglycemia, hyperglycemia, hyponatremia, hypoxia, uremia encephalopathy and hepatic encephalopathy. Here we report a case of transient homonymous hemianopia and seizures in a patient with hyperosmolar non ketotic state which got completely reversed as euglycemia was achieved.

2021 ◽  
Vol 22 (7) ◽  
pp. 3566
Author(s):  
Chae Bin Lee ◽  
Soon Uk Chae ◽  
Seong Jun Jo ◽  
Ui Min Jerng ◽  
Soo Kyung Bae

Metformin is the first-line pharmacotherapy for treating type 2 diabetes mellitus (T2DM); however, its mechanism of modulating glucose metabolism is elusive. Recent advances have identified the gut as a potential target of metformin. As patients with metabolic disorders exhibit dysbiosis, the gut microbiome has garnered interest as a potential target for metabolic disease. Henceforth, studies have focused on unraveling the relationship of metabolic disorders with the human gut microbiome. According to various metagenome studies, gut dysbiosis is evident in T2DM patients. Besides this, alterations in the gut microbiome were also observed in the metformin-treated T2DM patients compared to the non-treated T2DM patients. Thus, several studies on rodents have suggested potential mechanisms interacting with the gut microbiome, including regulation of glucose metabolism, an increase in short-chain fatty acids, strengthening intestinal permeability against lipopolysaccharides, modulating the immune response, and interaction with bile acids. Furthermore, human studies have demonstrated evidence substantiating the hypotheses based on rodent studies. This review discusses the current knowledge of how metformin modulates T2DM with respect to the gut microbiome and discusses the prospect of harnessing this mechanism in treating T2DM.


2021 ◽  
Author(s):  
Xianglong Zhang ◽  
Ying Lei ◽  
Oliver Homann ◽  
Marina Stolina ◽  
Songli Wang ◽  
...  

Obesity and type 2 diabetes (T2D) remain major global healthcare challenges and developing therapeutics necessitate using nonhuman primate models. Here, we present transcriptomic and proteomic analyses of all the major organs of cynomolgus monkeys with spontaneous obesity or T2D in comparison to healthy controls. Molecular changes occur predominantly in the adipose tissues of individuals with obesity, while extensive expression perturbations among T2D individuals are observed in many tissues, such as the liver, kidney, brain, and heart. Immune response-related pathways are upregulated in obesity and T2D, whereas metabolism and mitochondrial pathways are downregulated. Incorporating human single-cell RNA sequencing findings corroborates the role of macrophages and monocytes in obesity. Moreover, we highlight some potential therapeutic targets including SLC2A1 and PCSK1 in obesity as well as SLC30A8 and SLC2A2 in T2D. Our findings provide insights into tissue-specific molecular foundations of obesity and T2D and reveal the mechanistic links between these two metabolic disorders.


2020 ◽  
Vol 4 (2) ◽  
pp. 1002-1005
Author(s):  
G.A. Proshchai ◽  
◽  
S.V. Dudarenko ◽  
A.S. Partcerniak ◽  
E.Yu. Zagarskikh ◽  
...  

Objective: To evaluate the possibility of using fibroblast growth factor 21 (FGF 21) as a marker of metabolic disorders and premature aging in polymorbid cardiovascular pathology. Research methods: 199 men aged 35-55 years who were stratified into 3 groups were examined: group A - 117 patients with type 2 diabetes mellitus (type 2 diabetes), polymorbid cardiovascular disease (PCVD), obesity, androgen deficiency and anxiety-depressive disorders (ADD); group B - 55 patients with PCVD, obesity and ADD; group C - control group (n = 27). The examination of patients included a laboratory study of the level of FGF 21, indicators of carbohydrate and lipid metabolism, hormonal status, as well as daily monitoring of blood pressure and ECG. Results and conclusions. When compared with the control group, the level of FGF 21 was 3 times higher in the presence of type 2 diabetes. The most intense increase in FGF 21 levels was observed in groups of patients with several diseases. An increase in the level of FGF 21 in young and middle-aged people is probably due to a compensatory reaction to the existing androgen deficiency, disorders of carbohydrate and lipid metabolism. Strong correlations between FGF 21 and glucose, HDL cholesterol, total testosterone, ALT, and SBP during the day allow FGF 21 to be considered an early marker of cardiovascular disease and premature aging (PA) in young and middle-aged people


2006 ◽  
Vol 163 (suppl_11) ◽  
pp. S183-S183
Author(s):  
C Zhang ◽  
M.A Williams ◽  
C.G Solomon ◽  
F.B Hu

2020 ◽  
Vol 295 (31) ◽  
pp. 10842-10856 ◽  
Author(s):  
Wen Liu ◽  
Ye Yin ◽  
Meijing Wang ◽  
Ting Fan ◽  
Yuyu Zhu ◽  
...  

Chronic low-grade inflammation plays an important role in the pathogenesis of type 2 diabetes. Src homology 2 domain-containing tyrosine phosphatase-2 (SHP2) has been reported to play diverse roles in different tissues during the development of metabolic disorders. We previously reported that SHP2 inhibition in macrophages results in increased cytokine production. Here, we investigated the association between SHP2 inhibition in macrophages and the development of metabolic diseases. Unexpectedly, we found that mice with a conditional SHP2 knockout in macrophages (cSHP2-KO) have ameliorated metabolic disorders. cSHP2-KO mice fed a high-fat diet (HFD) gained less body weight and exhibited decreased hepatic steatosis, as well as improved glucose intolerance and insulin sensitivity, compared with HFD-fed WT littermates. Further experiments revealed that SHP2 deficiency leads to hyperactivation of caspase-1 and subsequent elevation of interleukin 18 (IL-18) levels, both in vivo and in vitro. Of note, IL-18 neutralization and caspase-1 knockout reversed the amelioration of hepatic steatosis and insulin resistance observed in the cSHP2-KO mice. Administration of two specific SHP2 inhibitors, SHP099 and Phps1, improved HFD-induced hepatic steatosis and insulin resistance. Our findings provide detailed insights into the role of macrophagic SHP2 in metabolic disorders. We conclude that pharmacological inhibition of SHP2 may represent a therapeutic strategy for the management of type 2 diabetes.


RSC Advances ◽  
2020 ◽  
Vol 10 (21) ◽  
pp. 12166-12182
Author(s):  
Anchala Kumari ◽  
Pallavi Somvanshi ◽  
Abhinav Grover

Large numbers of neurological and metabolic disorders occurring in humans are induced by the aberrant growth of aggregated or misfolded proteins.


2018 ◽  
Vol 9 (7) ◽  
pp. 3732-3742 ◽  
Author(s):  
Chun Chen ◽  
Li-Jun You ◽  
Qiang Huang ◽  
Xiong Fu ◽  
Bin Zhang ◽  
...  

Increasing evidence indicates that gut microbiota is an important factor in mediating the development of metabolic disorders, especially type 2 diabetes.


2019 ◽  
Vol 121 (12) ◽  
pp. 1365-1375 ◽  
Author(s):  
Edna S. Costa ◽  
Carolina N. França ◽  
Francisco A. H. Fonseca ◽  
Juliana T. Kato ◽  
Henrique T. Bianco ◽  
...  

AbstractDiabetes mellitus is a global epidemic, characterised as a heterogeneous group of metabolic disorders associated with high risk of CVD. Green banana biomass, which is composed of resistant starches (RS) and cannot be hydrolysed by amylases, delays gastric emptying and modulates insulin sensitivity, thus contributing to improve metabolic disorders. The aim of the present study was to investigate the effects of consumption of RS from green banana biomass on body composition, fasting plasma glucose, glycated Hb (HbA1c) and homeostasis model assessment of insulin resistance in subjects with pre-diabetes or type 2 diabetes on top of treatment. Middle-aged subjects (n113) of both sexes with pre-diabetes (HbA1c: 5·7–6·4 %) or diabetes (HbA1c ≥ 6·5 %) were randomised to receive nutritional support plus green banana biomass (40 g) (RS: approximately 4·5 g, G1,n62) or diet alone (G2,n51) for 24 weeks. Body composition, biochemical analyses and dietary intake were evaluated at the beginning and end of the study. In the experimental group (G1), consumption of RS was associated with reduction in HbA1c (P= 0·0001), fasting glucose (P= 0·021), diastolic blood pressure (P= 0·010), body weight (P= 0·002), BMI (P= 0·006), waist and hip circumferences (P< 0·01), fat mass percentage (P= 0·001) and increase in lean mass percentage (P= 0·011). In controls (G2), reductions were observed in waist and hip circumferences (P< 0·01), HbA1c (P= 0·002) and high-density lipoprotein-cholesterol (P= 0·020). In pre-diabetes or diabetes, non-significant differences were observed in the percentage reduction in HbA1c and fasting glucose in exploratory analyses. Our results indicate that the consumption of bioactive starches is a good dietary strategy to improve metabolic control and body composition.


2009 ◽  
Vol 425 (1) ◽  
pp. 41-52 ◽  
Author(s):  
Meilian Liu ◽  
Feng Liu

Adiponectin is an adipose-tissue-derived hormone with anti-diabetic, anti-atherogenic and anti-inflammatory functions. Adiponectin circulates in the bloodstream in trimeric, hexameric and high-molecular-mass species, and different forms of adiponectin have been found to play distinct roles in the regulation of energy homoeostasis. The serum levels of adiponectin are negatively correlated with obesity and insulin resistance, yet the underlying mechanisms remain elusive. In the present review, we summarize recent progress made on the mechanisms regulating adiponectin gene transcription, multimerization and secretion. We also discuss the potential relevance of these studies to the development of new clinical therapy for insulin resistance, Type 2 diabetes and other obesity-related metabolic disorders.


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