scholarly journals Mediation of Endogenous β-Endorphin in the Plasma Glucose-Lowering Action of Herbal Products Observed in Type 1-Like Diabetic Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
I. M. Liu ◽  
J. T. Cheng
Keyword(s):  
Adrenal Gland ◽  
Glucose Homeostasis ◽  
Plasma Glucose ◽  
Biological Effects ◽  
Diabetic Rats ◽  
Herbal Products ◽  
Peripheral Tissues ◽  
Glucose Lowering ◽  
Stimulation Of

Recently, there have been advances in the development of new substances effective in managing diabetic disorders. Opioid receptors couple multiple systems to result in various biological effects, although opioids are best known for analgesia. In the present review, we used our recent data to describe the advance in plasma glucose-lowering action of herbal products, especially the mediation of β-endorphin in glucose homeostasis of insulin-deficient diabetes. In type 1-like streptozotocin-induced diabetic rats, we identified many products purified from herbs that show a dose-dependent plasma glucose-lowering action. Increase in β-endorphin secretion from the adrenal gland may activate peripheral opioid μ-receptors (MOR) to enhance the expression of muscle glucose transporters and/or to reduce hepatic gluconeogenesis at the gene level, thereby leading to improved glucose utilization in peripheral tissues for amelioration of severe hyperglycemia. It has also been observed that stimulation of α1-adrenoceptors (α1-ARs) in the adrenal gland by some herbal products is responsible for the increase in β-endorphin secretion via a phospholipase C-protein kinase dependent pathway. However, an increase in β-endorphin secretion from the adrenal gland by herbal products can function via another receptor. New insights into the mediation of endogenous β-endorphin activation of peripheral MOR by herbal products for regulation of glucose homeostasis without the presence of insulin have been established. Therefore, an increase in β-endorphin secretion and/or direct stimulation of peripheral MOR via an insulin-independent action might serve as the potential target for development of a therapeutic agent or promising adjuvant in intensive plasma glucose control.

Effect of exercise training on glucose homeostasis in normal and insulin-deficient diabetic rats

1988 ◽  
Vol 65 (2) ◽  
pp. 844-851 ◽  
Author(s):  
L. J. Goodyear ◽  
M. F. Hirshman ◽  
S. M. Knutson ◽  
E. D. Horton ◽  
E. S. Horton
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Glucose Tolerance ◽  
Glucose Uptake ◽  
Glucose Homeostasis ◽  
Plasma Glucose ◽  
Citrate Synthase ◽  
Diabetic Rats ◽  
Oral Glucose ◽  
Oral Glucose Tolerance

The effect of 8-wk of treadmill training on plasma glucose, insulin, and lipid concentrations, oral glucose tolerance, and glucose uptake in the perfused hindquarter of normal and streptozocin-treated, diabetic Sprague-Dawley rats was studied. Diabetic rats with initial plasma glucose concentrations of 200-450 mg/dl and control rats were divided into trained and sedentary subgroups. Training resulted in lower plasma free fatty acid concentrations and increased triceps muscle citrate synthase activity in both the control and diabetic rats; triglyceride concentrations were lowered by training only in the diabetic animals. Oral glucose tolerance and both basal and insulin-stimulated glucose uptake in hindquarter skeletal muscle were impaired in the diabetic rats, and plasma glucose concentrations (measured weekly) gradually increased during the experiment. Training did not improve the hyperglycemia, impaired glucose tolerance, or decreased skeletal muscle glucose uptake in the diabetic rats, nor did it alter these parameters in the normal control animals. In considering our results and those of previous studies in diabetic rats, we propose that exercise training may improve glucose homeostasis in animals with milder degrees of diabetes but fails to cause improvement in the more severely insulin-deficient, diabetic rat.

The plasma glucose lowering action of tetrandrine in streptozotocin-induced diabetic rats

2004 ◽  
Vol 56 (5) ◽  
pp. 643-648 ◽  
Author(s):  
W. C. Chen ◽  
S. Hayakawa ◽  
T. Yamamoto ◽  
L. W. Huang ◽  
J. T. Cheng ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Diabetic Rats ◽  
Glucose Lowering

scholarly journals Novel Mechanism for Plasma Glucose-Lowering Action of Metformin in Streptozotocin-Induced Diabetic Rats

Diabetes ◽  
2006 ◽  
Vol 55 (3) ◽  
pp. 819-825 ◽  
Author(s):  
J.-T. Cheng ◽  
C.-C. Huang ◽  
I-M. Liu ◽  
T.-F. Tzeng ◽  
C. J. Chang
Keyword(s):  
Plasma Glucose ◽  
Diabetic Rats ◽  
Glucose Lowering

scholarly journals Plasma Glucose-Lowering Effect of Tramadol in Streptozotocin-Induced Diabetic Rats

Diabetes ◽  
2001 ◽  
Vol 50 (12) ◽  
pp. 2815-2821 ◽  
Author(s):  
J.-T. Cheng ◽  
I-M. Liu ◽  
T.-C. Chi ◽  
T.-F. Tzeng ◽  
F.-H. Lu ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Diabetic Rats ◽  
Glucose Lowering ◽  
Lowering Effect ◽  
Glucose Lowering Effect

Comparison of the glucose-lowering properties of vanadyl sulfate and bis(maltolato)oxovanadium(IV) following acute and chronic administration

1995 ◽  
Vol 73 (1) ◽  
pp. 55-64 ◽  
Author(s):  
Violet G. Yuen ◽  
J. H. McNeill ◽  
C. Orvig
Keyword(s):  
Oral Administration ◽  
Dose Response ◽  
Plasma Glucose ◽  
Intraperitoneal Injection ◽  
Chronic Administration ◽  
Diabetic Rats ◽  
Vanadyl Sulfate ◽  
Oral Gavage ◽  
Glucose Lowering ◽  
Glucose Levels

Numerous studies, both in vitro and in vivo, have demonstrated the insulin-mimetic properties of vanadium. Chronic oral administration of inorganic and organic compounds of both vanadium(IV) and vanadium(V) reduced plasma glucose levels and restored plasma lipid levels in streptozotocin-diabetic rats. We investigated the acute effects of both vanadyl sulfate and bis(maltolato)oxovanadium(IV) (BMOV), an organic vanadium compound, on plasma glucose levels by several routes of administration. Previous studies have shown that chronic administration of vanadyl sulfate has resulted in a sustained euglycemia following withdrawal of the drug. This effect was not observed following the chronic administration of BMOV; therefore, we investigated the effect of increasing the concentration of BMOV on the production of a sustained euglycemic response. An acute plasma glucose lowering effect was obtained with both vanadyl sulfate and BMOV when administered as a single dose by either oral gavage or intraperitoneal injection. In those animals that responded to vanadium treatment, plasma glucose levels were within the normal range within 2 to 6 h when given by i.p. injection or within 4 to 8 h when given by oral gavage. BMOV-treated rats that responded to treatment maintained the euglycemic effect for extended periods, ranging from 1 to 14 weeks following administration. However, vanadyl sulfate treated rats reverted to hyperglycemia within 12 to 24 h, depending on the route of administration. Intravenous administration of BMOV was effective in lowering plasma glucose levels only when administered by continuous infusion. An oral dose – response curve showed that BMOV was 2 to 3 times as potent as vanadyl sulfate. This difference in potency was observed with both oral and intraperitoneal administration, which suggests that the increase in potency with BMOV cannot be totally attributed to increased gastrointestinal absorption. Organic chelation of vanadium may facilitate uptake into vanadium-sensitive tissues. Chronic oral administration of higher concentrations of BMOV did not result in a sustained reduction in plasma glucose following withdrawal of the drug. All diabetic rats eventually responded to increased concentrations of BMOV with a restoration of plasma glucose levels to normal values; however, reversion to the hyperglycemic state occurred within 2 days of withdrawal of treatment. Chronic oral administration of BMOV did not produce a sustained euglycemic effect following withdrawal, but acute administrations of the compound by either oral gavage or intraperitoneal injection did produce a long-term reduction in plasma glucose levels. Rats treated chronically with vanadyl sulfate remained euglycemic even after the drug was withdrawn. However, acute treatment produced only a transient euglycemia.Key words: streptozotocin diabetic, acute, bis(maltolato)oxovanadium(IV), vanadyl sulfate, dose response.

Metformin can Activate Imidazoline I-2 Receptors to Lower Plasma Glucose in Type 1-like Diabetic Rats

2010 ◽  
Vol 43 (01) ◽  
pp. 26-30 ◽  
Author(s):  
J.-P. Lee ◽  
W. Chen ◽  
H.-T. Wu ◽  
K.-C. Lin ◽  
J.-T. Cheng
Keyword(s):  
Plasma Glucose ◽  
Diabetic Rats ◽  
Lower Plasma ◽  
Lower Plasma Glucose

scholarly journals Tissue-Specific Effects of Leptin on Glucose and Lipid Metabolism

2020 ◽  
Author(s):  
Sandra Pereira ◽  
Daemon L Cline ◽  
Maria M Glavas ◽  
Scott D Covey ◽  
Timothy J Kieffer
Keyword(s):  
Body Weight ◽  
Therapeutic Potential ◽  
Peripheral Tissues ◽  
Glucose Lowering ◽  
Glucose And Lipid Metabolism ◽  
Specific Effects ◽  
Regulate Body Weight ◽  
Activation Status

Abstract The discovery of leptin was intrinsically associated with its ability to regulate body weight. However, the effects of leptin are more far-reaching and include profound glucose-lowering and anti-lipogenic effects, independent of leptin’s regulation of body weight. Regulation of glucose metabolism by leptin is mediated both centrally and via peripheral tissues and is influenced by the activation status of insulin signaling pathways. Ectopic fat accumulation is diminished by both central and peripheral leptin, an effect that is beneficial in obesity-associated disorders. The magnitude of leptin action depends upon the tissue, sex, and context being examined. Peripheral tissues that are of particular relevance include the endocrine pancreas, liver, skeletal muscle, adipose tissues, immune cells, and the cardiovascular system. As a result of its potent metabolic activity, leptin is used to control hyperglycemia in patients with lipodystrophy and is being explored as an adjunct to insulin in patients with type 1 diabetes. To fully understand the role of leptin in physiology and to maximize its therapeutic potential, the mechanisms of leptin action in these tissues needs to be further explored.

scholarly journals Marked and rapid decreases of circulating leptin in streptozotocin diabetic rats: reversal by insulin

1998 ◽  
Vol 274 (5) ◽  
pp. R1482-R1491 ◽  
Author(s):  
Peter J. Havel ◽  
Janet Y. Uriu-Hare ◽  
Tina Liu ◽  
Kimber L. Stanhope ◽  
Judith S. Stern ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Subcutaneous Insulin ◽  
Glucose Lowering ◽  
Streptozotocin Diabetic Rats ◽  
Plasma Leptin

Evidence for regulation of circulating leptin by insulin is conflicting. Diabetes was induced in rats with streptozotocin (STZ; 40 mg ⋅ kg−1⋅ day−1× 2 days) to examine the effect of insulin-deficient diabetes and insulin treatment on circulating leptin. After 12 wk, plasma leptin concentrations in untreated rats were all <0.4 ng/ml versus 4.9 ± 0.9 ng/ml in control animals ( P < 0.005). In rats treated with subcutaneous insulin implants for 12 wk, which reduced hyperglycemia by ∼50%, plasma leptin was 2.1 ± 0.6 ng/ml, whereas leptin concentrations were 6.0 ± 1.6 ng/ml in insulin-implanted rats receiving supplemental injections of insulin for 4 days to normalize plasma glucose ( P< 0.005 vs. STZ untreated). In a second experiment, plasma leptin was monitored at biweekly intervals during 12 wk of diabetes. In rats treated with insulin implants, plasma leptin concentrations were inversely proportional to glycemia ( r= −0.64; P < 0.0001) and unrelated to body weight ( P = 0.40). In a third experiment, plasma leptin concentrations were examined very early after the induction of diabetes. Within 24 h after STZ injection, plasma insulin decreased from 480 ± 30 to 130 ± 10 pM ( P < 0.0001), plasma glucose increased from 7.0 ± 0.2 to 24.8 ± 0.5 mM, and plasma leptin decreased from 3.2 ± 0.2 to 1.2 ± 0.1 ng/ml (Δ = −63 ± 3%, P < 0.0001). In a subset of diabetic rats treated with insulin for 2 days, glucose decreased to 11.7 ± 3.9 mM and leptin increased from 0.5 ± 0.1 to 2.9 ± 0.6 ng/ml ( P< 0.01) without an effect on epididymal fat weight. The change of leptin was correlated with the degree of glucose lowering ( r = 0.75, P < 0.05). Thus insulin-deficient diabetes produces rapid and sustained decreases of leptin that are not solely dependent on weight loss, whereas insulin treatment reverses the hypoleptinemia. We hypothesize that decreased glucose transport into adipose tissue may contribute to decreased leptin production in insulin-deficient diabetes.

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