PURPOSE: This study aimed to determine the impaired glucose tolerance and diabetes prevalence in patients with essential hypertension (HT) and to compare the developed microvascular complications of these groups. MATERIALS AND METHODS: An oral glucose tolerance test (OGTT) was performed on 338 essential hypertensive cases and glucose tolerances were classified according to ADA-2002 criteria. RESULTS: Of the 338 cases, 32 people had diabetes (DM, 9.46%), 78 people had glucose intolerance (IGT, 23.1%), and 228 people had only hypertension but not IGT and DM (67.4%). Both the mean ages of the DM group (56.9 +/- 6.7 years, p = 0.002) and IGT group (56.3 +/- 8.4 years, p = 0.003) were older than the mean age of the control group (51.1 +/- 6.4 years). The risk of IGT development was found to be four times greater in male cases than female cases when compared to the control group (p = 0.004, add ratio = 4.194). There were no significant differences in the body mass indexes (BMI's), hypertension durations, and microvascular complications between the groups. CONCLUSION: In conclusion, the risk of IGT and DM development in hypertensive cases increases with aging and longer hypertension duration. The risk of IGT development in hypertensive cases is four times more in males.
Aged ; Blood Glucose ; Diabetes Mellitus, Type 2/pathology/physiopathology ; Female ; Glucose Intolerance/pathology/*physiopathology ; Humans ; Hypertension/pathology/*physiopathology ; Male ; Middle Aged

This article reviews the clinical and experimental researches on cognitive impairment related to diabetes in the recent decade. Most clinical studies indicate that the cognitive impairment in patients with type 1 diabetes mellitus is related to recurrent hypoglycemia closely. There is little research about whether or not hyperglycemia is related to cognitive impairment in patients with type 1 diabetes mellitus. Most studies indicate that the cognitive impairment in type 2 diabetes involves multiple factors through multiple mechanisms, including blood glucose, blood lipid, blood pressure, level of insulin, medication, chronic complication, etc. But, there has been no large-scale, multi-center, randomized controlled clinical trial in China recently. And what is more, some problems exist in this field of research, such as the lack of golden criterion of cognitive function measurement, different population of studied objects, and incomprehensive handling of confounding factors. Experimental studies found that hippocampal long-term potentiation (LTP) was impaired, which were manifested by impairment of spatial memory and decreased expression of LTP, but it's relation to hyperglycemia, the duration of diabetes, learning and memory has always been differently reported by different researches. Thus, there are a lot of unknown things to be explored and studied in order to clarify its mechanism. TCM has abundant clinical experience in treating cerebral disease with medicine that enforces the kidney and promotes wit. However, there has been no research on treating diabetic cognitive impairment, which requires work to be done actively and TCM to be put into full play, in order to improve the treatment of diabetes and enhance living quality of patients.
Animals ; Cognition Disorders ; etiology ; pathology ; physiopathology ; Diabetes Mellitus, Experimental ; pathology ; physiopathology ; psychology ; Diabetes Mellitus, Type 1 ; pathology ; physiopathology ; psychology ; Diabetes Mellitus, Type 2 ; pathology ; physiopathology ; psychology ; Drugs, Chinese Herbal ; therapeutic use ; Hippocampus ; pathology ; physiopathology ; Humans ; Hyperglycemia ; complications ; Hypoglycemia ; complications ; Long-Term Potentiation ; Neuronal Plasticity

Endothelial dysfunction contributes to cardiovascular diseases that are also characterized by insulin resistance. Insulin resistance is a hallmark of metabolic disorders including Type 2 diabetes, obesity, and the metabolic syndrome that are also characterized by endothelial dysfunction. Metabolic actions of insulin to promote glucose disposal are augmented by vascular actions of insulin in endothelium to stimulate production of the vasodilator nitric oxide (NO). Indeed, NO-dependent increases in blood flow to skeletal muscle account for 25% to 40% of the increase in glucose uptake in response to insulin stimulation. PI 3-kinase-dependent insulin signaling pathways in endothelium related to production of NO share striking similarities with metabolic pathways in skeletal muscle that promote glucose uptake. Other distinct non-metabolic branches of insulin signaling pathways regulate secretion of the vasoconstrictor endothelin-1 (ET-1) in endothelium. Metabolic insulin resistance is characterized by pathway-specific impairment in PI 3-kinase-dependent signaling that in endothelium may cause imbalance between production of NO and secretion of ET-1 leading to decreased blood flow that worsens insulin resistance. Therapeutic interventions in both animal models and human studies demonstrate that improving endothelial function ameliorates insulin resistance while improving insulin sensitivity ameliorates endothelial dysfunction. Taken together, cellular, physiological, clinical, and epidemiological studies strongly support a reciprocal relationship between endothelial dysfunction and insulin resistance that helps to link cardiovascular and metabolic diseases. In this review, pathophysiological mechanisms that couple endothelial dysfunction with insulin resistance will be discussed with an emphasis on important therapeutic implications for the metabolic syndrome.
Animals ; Diabetes Mellitus, Type 2 ; physiopathology ; Endothelium, Vascular ; physiopathology ; Glucose ; metabolism ; Humans ; Hypertension ; metabolism ; pathology ; Insulin ; metabolism ; Insulin Resistance ; Metabolic Syndrome ; physiopathology ; Nitric Oxide ; metabolism

OBJECTIVETo observe the characteristics of coronary microvascular lesions (CML) in the autopsied elderly cases with hypertensive left ventricular hypertrophy (LVH) and the difference of CML among the groups of essential hypertension (EHT), coronary heart disease (CHD) and diabetes (NIDDM) also with LVH.

METHODSA retrospective study was performed in 206 cases > or = 60 years old of EHT, CHD and NIDDM with LVH and 30 normal cases as control, out of 3195 consecutive autopsied cases from 1954 to 1996 in our hospital. Arterioles with diameters of 10 - 60 microm and capillaries in the muscular layer were shown by the methods of HE, Elastic fiber + VG staining and immunohistochemistry of CD31. Quantitative measurements on the arteriole density (AD), the ratio of arteriolar wall and cavity (RWC), capillary density (CD) and the area of endothelial cell (AEC) were performed with light microscope observation and image analysis by computer. According to the thickness of the left ventricle free wall, the severity of LVH was divided into four degrees from 0 to III. LVH of degree 0-III was observed in EHT group, while only LVH of degree I was found in CHD, EHT + CHD, and NIDDM groups. SAS system was used for statistical analysis.

RESULTSAD and RWC increased while CD and AEC decreased significantly with the progression of LVH in EHT groups (P < 0.05 - 0.01). There was a similar but more severe change in the (HT + CHD) group (P < 0.01); the AD increased (P < 0.05) while all other measurements did not show obvious changes in the CHD group. The AD increased, CD and AEC decreased (all P < 0.05), but RWC did not change very much in the NIDDM group.

CONCLUSIONCML in the EHT group was characterized by an increased AD and RWC, decreased CD and AEC, among which the increased RWC was the typical change in EHT groups compared with the groups of CHD and NIDDM. Damaged CML may be one of the main factors for decreased coronary flow reserve and myocardial ischemia in cases of EHT with LVH.

Aged ; Autopsy ; Coronary Circulation ; Coronary Disease ; complications ; pathology ; physiopathology ; Coronary Vessels ; pathology ; physiopathology ; Diabetes Mellitus, Type 2 ; complications ; pathology ; physiopathology ; Female ; Humans ; Hypertension ; complications ; pathology ; physiopathology ; Hypertrophy, Left Ventricular ; complications ; pathology ; physiopathology ; Male ; Middle Aged

BACKGROUNDIntensive insulin therapy has been found to lessen the progress of diabetic retinopathy (DR) to some extent, while it has also been implicated to be responsible for decrease of DR. We investigated visual function and morphological changes in the macular area in short-term follow-up of patients with type 2 diabetes mellitus after intensive insulin therapy.

METHODSThis was a prospective clinical study of nonproliferative DR patients (102 eyes, 120 patients) undergoing intensive insulin therapy. The Contrast Glare Tester (Takagi CGT-1000) was used to examine contrast sensitivity (CS) and Heidelberg Retina Tomograph (HRT) II and Stratus Model 3000 OCT were used to observe the changes of morphology in the macular area. Follow-up times were pre-intensive therapy, 3 and 6 months post-intensive therapy.

RESULTSCS at low and middle frequencies was higher at 3 and 6 months post-therapy compared with pre-therapy (P < 0.05). Significant differences in CS at low frequency were found between 6 and 3 months post-therapy (P < 0.05). Macular edema index was lower in the first, second, and third rings of the macular area after intensive therapy compared with pre-therapy (P < 0.05). Compared with 3 months post-therapy, the macular edema index was lower in the first, second, and third rings of the macular area at 6 months post-therapy (P > 0.05). No significant differences in the thickness of the first, second, and third rings of the macular area were detected between 3 and 6 months post-therapy and pre-therapy (P > 0.05).

CONCLUSIONCS and macular edema indexes were significantly improved in nonproliferative diabetic retinopathy patients after intensive insulin therapy, but thickness of the macular area was unchanged.

Diabetes Mellitus, Type 2 ; drug therapy ; pathology ; physiopathology ; Follow-Up Studies ; Humans ; Insulin ; therapeutic use ; Macula Lutea ; pathology ; Middle Aged ; Prospective Studies ; Tomography, Optical Coherence ; Vision, Ocular ; physiology

BACKGROUNDLittle attention has been paid to the role of subcortical deep gray matter (SDGM) structures in type 2 diabetes mellitus (T2DM)-induced cognitive impairment, especially hippocampal subfields. Our aims were to assess the in vivo volumes of SDGM structures and hippocampal subfields using magnetic resonance imaging (MRI) and to test their associations with cognitive performance in T2DM.

METHODSA total of 80 T2DM patients and 80 neurologically unimpaired healthy controls matched by age, sex and education level was enrolled in this study. We assessed the volumes of the SDGM structures and seven hippocampal subfields on MRI using a novel technique that enabled automated volumetry. We used Mini-Mental State Examination and Montreal Cognitive Assessment (MoCA) scores as measures of cognitive performance. The association of glycosylated hemoglobin (HbA1c) with SDGM structures and neuropsychological tests and correlations between hippocampal subfields and neuropsychological tests were assessed by partial correlation analysis in T2DM.

RESULTSBilaterally, the hippocampal volumes were smaller in T2DM patients, mainly in the CA1 and subiculum subfields. Partial correlation analysis showed that the MoCA scores, particularly those regarding delayed memory, were significantly positively correlated with reduced hippocampal CA1 and subiculum volumes in T2DM patients. Additionally, higher HbA1c levels were significantly associated with poor memory performance and hippocampal atrophy among T2DM patients.

CONCLUSIONSThese data indicate that the hippocampus might be the main affected region among the SDGM structures in T2DM. These structural changes in the hippocampal CA1 and subiculum areas might be at the core of underlying neurobiological mechanisms of hippocampal dysfunction, suggesting that degeneration in these regions could be responsible for memory impairments in T2DM patients.

Aged ; CA1 Region, Hippocampal ; pathology ; physiopathology ; Diabetes Mellitus, Type 2 ; pathology ; physiopathology ; Female ; Hippocampus ; pathology ; physiopathology ; Humans ; Magnetic Resonance Imaging ; Male ; Memory Disorders ; etiology ; pathology ; Middle Aged ; Neuropsychological Tests

OBJECTIVETo observe the dynamic expression of calcium-sensing receptor(CaSR) in myocardium of diabetic rats.

METHODSThirty male Wistar rats were randomly divided into 3 groups including control, diabetic-4 week and diabetic-8 week groups(n = 10). The type 2 diabetes mellitus models were established by intraperitoneal injection of streptozotocin (STZ, 30 mg/kg) after high-fat and high-sugar diet for one month. The cardiac morphology was observed by electron microscope. Western blot analyzed the expression of CaSR, phospholamban (PLN), a calcium handling regulator, and Ca+-ATPase(SERCA) in cardiac tissues.

RESULTSCompared with control group, the expressions of CaSR and SERCA were decreased, while the expression of PLN was significantly increased in a time-dependent manner in diabetic groups. Meanwhile diabetic rats displayed abnormal cardiac structure.

CONCLUSIONThese results indicate that the CaSR expression of myocardium is reduced in the progression of DCM, and its potential mechanism may be related to the imnaired intracellular calcium homeostasis.

Animals ; Calcium-Binding Proteins ; metabolism ; Diabetes Mellitus, Experimental ; complications ; Diabetes Mellitus, Type 2 ; Diabetic Cardiomyopathies ; metabolism ; physiopathology ; Disease Progression ; Heart ; physiopathology ; Male ; Myocardium ; metabolism ; pathology ; Rats ; Rats, Wistar ; Receptors, Calcium-Sensing ; metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; metabolism ; Streptozocin

β-cell failure coupled with insulin resistance plays a key role in the development of type 2 diabetes mellitus (T2DM). Changed adipokines in circulating level form a remarkable link between obesity and both β-cell failure and insulin resistance. Some adipokines have beneficial effects,whereas others have detrimental properties. The overall contribution of adipokines to β-cell failure mainly depends on the interactions among adipokines. This article reviews the role of individual adipokines such as leptin,adiponectin,and resistin in the function,proliferation,death,and failure of β-cells. Future studies focusing on the combined effects of adipokines on β-cells failure may provide new insights in the treatment of T2DM.
Adipokines ; metabolism ; Adiponectin ; metabolism ; Diabetes Mellitus, Type 2 ; physiopathology ; Humans ; Insulin Resistance ; Insulin-Secreting Cells ; pathology ; Leptin ; metabolism ; Obesity ; Resistin ; metabolism

OBJECTIVETo investigate the perfusion restoration of type 1 diabetic mouse under the setting of surgically induced hind limb ischemia and the number and function of bone marrow endothelial progenitor cells (EPCs).

METHODSForty mice were randomly divided into two groups: one group was injected with alloxan through tail vein to induce type 1 diabetes mellitus, and another group was set as control group. All mice were surgically induced to hind limb ischemia. Blood flow was monitored with Laser Doppler perfusion imaging for 4 weeks after artery ligation. Ten mice in each group were sacrificed and muscle tissues were harvested for histological detection. The remaining mice were sacrificed 7 days after surgery, bone marrow mesenchymal stem cells were harvested and EPCs were analyzed by flow cytometry and then were collected to culture for functional detection.

RESULTSAll mice received alloxan injection showed typical symptoms of type 1 diabetes mellitus. Restoration of blood flow was significantly slower in type 1 diabetic mice with lower level of vascular density in ischemic muscles than control group (P < 0.001, P < 0.05). The number and function of EPCs (CD34 and vascular endothelial growth factor receptor 2 double positive cells) in type 1 diabetic mice were significantly lower than that in control mice (P < 0.05).

CONCLUSIONSThe spontaneous angiogenesis is attenuated with a decreased number and function of EPCs in the setting of type 1 diabetes mellitus. This may partly explain why diabetic patients with peripheral artery diseases have more aggressive disease and poorer outcome.

Animals ; Antigens, CD34 ; analysis ; Cell Count ; Diabetes Mellitus, Experimental ; complications ; pathology ; Diabetes Mellitus, Type 1 ; complications ; Hindlimb ; blood supply ; Ischemia ; complications ; physiopathology ; Mesenchymal Stromal Cells ; chemistry ; Mice ; Reperfusion ; Vascular Endothelial Growth Factor Receptor-2 ; analysis

Correlation between the intrahepatic inflammatory pathogenesis and the TCM theory of liver collateral injury by toxins in patients of type 2 diabetes mellitus (T2DM) with insulin resistance (IR) was investigated, to elucidate that removing toxins, dredging collateral and modulating Gan could be one of the effective approaches for inhibiting intrahepatic inflammation mechanism of T2DM with IR.
Chemokine CCL2 ; metabolism ; Diabetes Mellitus, Type 2 ; complications ; metabolism ; physiopathology ; Diagnosis, Differential ; Humans ; Inflammation ; etiology ; metabolism ; physiopathology ; Insulin Resistance ; Liver ; metabolism ; pathology ; physiopathology ; Medicine, Chinese Traditional ; NF-kappa B ; metabolism