scholarly journals Angiotensin type-1 receptor blockade with losartan increases insulin sensitivity and improves glucose homeostasis in subjects with type 2 diabetes and nephropathy

2007 ◽  
Vol 22 (7) ◽  
pp. 1943-1949 ◽  
Author(s):  
H.-M. Jin ◽  
Y. Pan
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Homeostasis ◽  
Receptor Blockade ◽  
Angiotensin Type

scholarly journals Association between breastfeeding and insulin sensitivity among young people with Type 1 and Type 2 diabetes: the SEARCH Nutrition Ancillary Study

2016 ◽  
Vol 33 (10) ◽  
pp. 1452-1455
Author(s):  
N. S. The ◽  
C. M. Shay ◽  
A. P. Lamichhane ◽  
T. L. Crume ◽  
J. L. Crandell ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Young People ◽  
Ancillary Study

Angiotensin type 2 receptors mediate depressor phase of biphasic pressure response to angiotensin

1993 ◽  
Vol 264 (5) ◽  
pp. R917-R923 ◽  
Author(s):  
D. A. Scheuer ◽  
M. H. Perrone
Keyword(s):  
Pressor Response ◽  
Pressure Response ◽  
Receptor Blockade ◽  
At1 Receptors ◽  
Angiotensin Iii ◽  
Depressor Action ◽  
Angiotensin Type ◽  
At2 Receptors

Angiotensin (ANG) can produce a biphasic arterial pressure response, i.e., an increase followed by a decrease. Because ANG type 1 (AT1) receptors mediate the pressor response to ANG, we hypothesized that the opposing depressor action is mediated by the ANG type 2 (AT2) receptors. In thiobutabarbital (Inactin)-anesthetized rats bolus injections of angiotensin III (ANG III; 100, 300, and 1,000 ng/kg iv) produced peak increases in MAP at 20 s of 13.4 +/- 1.4, 20.1 +/- 2, and 27.5 +/- 2.8 mmHg and maximum decreases in pressure at 120 s of -6.3 +/- 1.5, -6.8 +/- 2.2, and -11.4 +/- 4.9 mmHg. During blockade of the AT1 receptors with DuP 753 (losartan, 10 mg/kg) the increases in MAP were eliminated (P < 0.01), whereas the depressor responses (-24.7 +/- 8, -32.8 +/- 9.3, and -42.0 +/- 10.0 mmHg) were significantly (P < 0.05) larger. In separate groups of rats, combined blockade of both AT1 and AT2 receptors eliminated all changes in MAP in response to ANG III, whereas blockade of AT2 receptors alone enhanced the pressor response to ANG III. During AT1 receptor blockade angiotensin II also caused consistent decreases in pressure, which were inhibited during combined blockade of AT1 and AT2 receptors. Therefore, we have demonstrated that the AT2 receptors mediate a depressor response to ANG.

scholarly journals METABOLIC PHENOTYPING GUIDELINES: Assessing glucose homeostasis in rodent models

2014 ◽  
Vol 222 (3) ◽  
pp. G13-G25 ◽  
Author(s):  
James E Bowe ◽  
Zara J Franklin ◽  
Astrid C Hauge-Evans ◽  
Aileen J King ◽  
Shanta J Persaud ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
Β Cells ◽  
Advantages And Disadvantages ◽  
Autoimmune Destruction ◽  
Normal Glucose

The pathophysiology of diabetes as a disease is characterised by an inability to maintain normal glucose homeostasis. In type 1 diabetes, this is due to autoimmune destruction of the pancreatic β-cells and subsequent lack of insulin production, and in type 2 diabetes it is due to a combination of both insulin resistance and an inability of the β-cells to compensate adequately with increased insulin release. Animal models, in particular genetically modified mice, are increasingly being used to elucidate the mechanisms underlying both type 1 and type 2 diabetes, and as such the ability to study glucose homeostasisin vivohas become an essential tool. Several techniques exist for measuring different aspects of glucose tolerance and each of these methods has distinct advantages and disadvantages. Thus the appropriate methodology may vary from study to study depending on the desired end-points, the animal model, and other practical considerations. This review outlines the most commonly used techniques for assessing glucose tolerance in rodents and details the factors that should be taken into account in their use. Representative scenarios illustrating some of the practical considerations of designingin vivoexperiments for the measurement of glucose homeostasis are also discussed.

Dissociation Of Glucose Homeostasis From Insulin Sensitivity In College-age Subjects At Risk For Type 2 Diabetes

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S310
Author(s):  
Dana Townsend ◽  
Mark D. Haub ◽  
Barbara J. Lutjemeier ◽  
Leonardo Ferreira ◽  
Allison J. Harper ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
At Risk ◽  
Insulin Sensitivity ◽  
Glucose Homeostasis ◽  
College Age

scholarly journals Insulin Sensitivity in the Offspring of Women With Type 1 and Type 2 Diabetes

Diabetes Care ◽  
2004 ◽  
Vol 27 (5) ◽  
pp. 1148-1152 ◽  
Author(s):  
W. A. Hunter ◽  
T. Cundy ◽  
D. Rabone ◽  
P. L. Hofman ◽  
M. Harris ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity

Relationship between Serum Butyrylcholinesterase Activity, Hypertriglyceridaemia and Insulin Sensitivity in Diabetes Mellitus

1993 ◽  
Vol 85 (1) ◽  
pp. 77-81 ◽  
Author(s):  
C. A. Abbott ◽  
M. I. MacKness ◽  
S. Kumar ◽  
A. O. Olukoga ◽  
C. Gordon ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Lipoprotein Metabolism ◽  
Diabetic Patients ◽  
Control Subjects ◽  
Triacylglycerol Concentration ◽  
Butyrylcholinesterase Activity

1. The activity of serum butyrylcholinesterase (‘pseudocholinesterase’, EC3.1.1.8) was investigated in 56 patients with type 1 diabetes mellitus, 51 patients with type 2 diabetes mellitus and 101 healthy control subjects. 2. Butyrylcholinesterase activity was significantly elevated in both type 1 (8.10 ± 3.35 units/ml) and type 2 (7.22 ± 1.95 units/ml) diabetes compared with the control subjects (4.23 ± 1.89 units/ml) (P <0.001). 3. In the patients with type 1 and type 2 diabetes, serum butyrylcholinesterase activity was correlated with log serum fasting triacylglycerol concentration (r = 0.41 and r = 0.43, respectively, P <0.001). In the type 2 population serum butyrylcholinesterase activity was also correlated with insulin sensitivity (r = −0.51, P <0.001). 4. Serum butyrylcholinesterase activity was unrelated to age, gender, serum γ-glutamyltranspeptidase activity, body mass index, or treatment for diabetes in both the diabetic populations. 5. In 37 non-diabetic patients with butyrylcholinesterase deficiency serum triacylglycerol levels were in the normal range. 6. These results are consistent with the view that butyrylcholinesterase may have a role in the altered lipoprotein metabolism in hypertriglyceridaemia associated with insulin insensitivity or insulin deficiency in diabetes mellitus.

scholarly journals Astrocyte Clocks and Glucose Homeostasis

2021 ◽  
Vol 12 ◽  
Author(s):  
Olga Barca-Mayo ◽  
Miguel López
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Circadian Clock ◽  
Glucose Homeostasis ◽  
Metabolic Diseases ◽  
Current Knowledge ◽  
Genetic Alterations ◽  
Whole Body

The endogenous timekeeping system evolved to anticipate the time of the day through the 24 hours cycle of the Earth’s rotation. In mammals, the circadian clock governs rhythmic physiological and behavioral processes, including the daily oscillation in glucose metabolism, food intake, energy expenditure, and whole-body insulin sensitivity. The results from a series of studies have demonstrated that environmental or genetic alterations of the circadian cycle in humans and rodents are strongly associated with metabolic diseases such as obesity and type 2 diabetes. Emerging evidence suggests that astrocyte clocks have a crucial role in regulating molecular, physiological, and behavioral circadian rhythms such as glucose metabolism and insulin sensitivity. Given the concurrent high prevalence of type 2 diabetes and circadian disruption, understanding the mechanisms underlying glucose homeostasis regulation by the circadian clock and its dysregulation may improve glycemic control. In this review, we summarize the current knowledge on the tight interconnection between the timekeeping system, glucose homeostasis, and insulin sensitivity. We focus specifically on the involvement of astrocyte clocks, at the organism, cellular, and molecular levels, in the regulation of glucose metabolism.

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