Roles of Daily Diet and Beta-Adrenergic System in the Treatment of Obesity and Diabetes

Author(s):  
Ebru Arioglu Inan ◽  
Belma Turan
1991 ◽  
Vol 17 (2) ◽  
pp. A133 ◽  
Author(s):  
Karil Bellah ◽  
Thomas Raya ◽  
Sheldon Litwin ◽  
Steven Goldman ◽  
Joel Karliner

2014 ◽  
Vol 31 (02) ◽  
pp. 123-127 ◽  
Author(s):  
S. Gupta ◽  
S. Kalra ◽  
V. Bharihoke ◽  
D. Dhurandhar

AbstractIn the present world people have become conscious of the fact that sugar is one of the commonest culprits for gain in weight and blood sugar in diabetes. One of the artificial sweetener, sucralose is widely used by diabetics is still under strict scrutiny because of the contradictory feedbacks obtained from various studies, often discouraging its use. Therefore, there arises a need to check whether the use of sucralose is safe or not. The present study was designed to determine to evaluate and compare the histological changes of sucralose on the islets of pancreas in albino rats. Methods: The adult Wistar albino rats were given sucralose orally by gavage in the dose of 3gms/kg body weight/day dissolved in distilled water and only distilled water for 30 days to experimental and control groups respectively. The animals were weighed prior to and after the experiment. The animals were sacrificed on day 31. The pancreas was dissected and observed grossly. Tissue was processed; paraffin blocks were prepared and 8 micron thick sections were cut. Sections were stained with Haemotoxylin and Eosin and Gomori's stains. Results: Pancreatic toxicity was observed in the form of vaculation of islets, lymphocytic infilterate, degeneration of islets and acini of Pancreas. The commonly used non-lethal dose of sucralose induced damage to Pancreas is startling. Conclusion: The results obtained have wide implications for nutrient sensing and nutrition in the treatment of obesity and diabetes.


Eating NAFTA ◽  
2018 ◽  
pp. 89-116
Author(s):  
Alyshia Gálvez

The fourth chapter, “NAFTA: Free Trade in the Body,” describes the magnitude and characteristics of Mexico’s so-called obesity and diabetes epidemic and the current hypotheses for the causes and treatment of obesity for individuals and at the population level. The chapter points out some of the lesser known hypotheses for the abrupt rise in obesity and diet-related chronic diseases in the last few decades. Far from linking the rise of obesity to increased appetites for snacks and sodas, some of these hypotheses focus on ways that the production and consumption of processed foods and beverages have increased people’s exposure to chemicals with metabolic and endocrinological properties that produce weight gain and alter organ function. The methodological and empirical challenges of understanding the effects of economic policy, like free trade agreements, on the body are explored.


Author(s):  
Gia Merlo

This chapter addresses the rise of lifestyle medicine. The impact of chronic diseases on health and quality of life are well-known within the medical community. Preventive medicine has only been partially successful in addressing these problems. For physicians to advocate healthy lifestyle choices for their patients, they must first understand what a healthy lifestyle entails. The Six Pillars of Lifestyle Medicine outline the six main lifestyle changes—healthful eating, increasing physical activity, improving sleep, managing stress, avoiding risky substances, forming and maintaining relationships—that physicians should promote to their patients. The global public health burden of diabetes, obesity, and other lifestyle diseases is increasing at an astounding rate. However, very few training programs have robust educational offerings for physicians on nonpharmacological treatment of obesity and diabetes.


1977 ◽  
Vol 43 (4) ◽  
pp. 612-616 ◽  
Author(s):  
R. J. Porcelli ◽  
A. T. Viau ◽  
N. E. Naftchi ◽  
E. H. Bergofsky

The role of the adrenergic receptor in mediating pulmonary vascular responses to gaseous and humoral agents was investigated by use of epinephrine injections in the perfused feline pulmonary circulation. Alteration of the balance between alpha- and beta-adrenergic activity was quantified by measurement of decreasing vasoconstrictor activity to epinephrine and rising lobar tissue 3′,5′-adenosine cyclic monophosphate (cAMP) levels. The increased beta-adrenergic activity thus generated was associated with marked reductions in the pulmonary vasoconstrictor responses to hypoxia, hypercapnic acidosis, and histamine, but not to serotonin. Repeated pulmonary vasodilations or increases in blood, but not pulmonary tissue, levels of cAMP induced by theophylline doses, which would not necessarily affect the beta-adrenergic activity, did not alter the pulmonary vasoconstrictor responses to hypoxia, hypercapnia, or histamine. These data support the significant role which the adrenergic system plays in mediating pulmonary vasoconstrictor responses to certain specific gaseous and humoral agents, and the specificity with which this mediation occurs serves to link hypoxia and histamine together so that the latter could serve as a mediator of the former.


2019 ◽  
Vol 30 (2) ◽  
pp. 219-232 ◽  
Author(s):  
Reham Z. Hamza ◽  
Rasha A. Al-Eisa ◽  
Amir E. Mehana ◽  
Nahla S. El-Shenawy

Abstract Background Aspartame (ASP) is used for treatment of obesity and diabetes mellitus. This study was designed to illustrate the biochemical responses and histopathological alterations besides the genotoxicity of ASP alone or with l-carnitine (LC) in the liver of rats. Methods Animals were separated into six groups: control, lower dose of ASP (ASP-LD; 75 mg/kg), higher dose of ASP (ASP-HD; 150 mg/kg), l-carnitine (LC; 10 mg/kg), ASP-LD plus LC, and ASP-HD plus LC. Treatment was carried out orally for 30 consecutive days. Results ASP raised the activity of some enzymes of liver markers and disturbed the lipid profile levels. The hepatic reduced glutathione (GSH) levels, the marker enzymes of antioxidant activities, were obviously diminished, and, possibly, the lipid peroxidation, C-reactive protein, and interleukins levels were increased. ASP significantly increased the DNA deterioration in comparison with the control in a dose-dependent manner. LC prevented ASP-induced liver damage as demonstrated by the enhancement of all the above parameters. Results of histopathological and electron microscopic examination proved the biochemical feedback and the improved LC effect on liver toxicity. Conclusions The co-treatment of LC showed different improvement mechanisms against ASP-induced liver impairment. So, the intake of ASP should be regulated and taken with LC when it is consumed in different foods or drinks to decrease its oxidative stress, histopathology, and genotoxicity of liver.


1989 ◽  
Vol 67 (1) ◽  
pp. 221-225 ◽  
Author(s):  
L. S. Lamont ◽  
D. G. Patel ◽  
S. C. Kalhan

This study examined the effects of a nonselective beta-blocking agent on whole-body leucine metabolism in humans. Five normal, healthy subjects (4 male, 1 female) underwent a 6-h primed, constant-rate infusion of L-[1–13C]leucine after 5 days of twice daily oral use of 80 mg propranolol and a placebo. Leucine turnover was determined by tracer dilution and leucine oxidation by 13C enrichment of the expired CO2. Propranolol decreased the total daily energy expenditure from 1,945 +/- 177.5 to 1,619 +/- 92.5 kcal/day (P less than 0.05). A fasting associated decrease in blood glucose and an attenuated rise in free fatty acids and ketones were observed during beta-blockade. Propranolol also increased plasma leucine concentrations (73.1 +/- 8.7 to 103.4 +/- 7.3 mumol/l; P less than 0.05) and leucine oxidation (13.2 +/- 1.2 to 17.1 +/- 1.3 mumol.kg-1.h-1; P less than 0.05), although leucine turnover was not significantly altered (100.5 +/- 7.3 vs. 126.0 +/- 12.3 mumol.kg-1.h-1). In addition, the urinary urea nitrogen-to-creatinine ratio was greater during propranolol administration (0.24 +/- 0.04 vs. 0.34 +/- 0.02 mol/g; P less than 0.05). These data suggest that the beta-adrenergic system plays a role in the modulation of whole-body leucine metabolism in humans. Whether these changes are the result of a direct effect on skeletal muscle or an indirect effect mediated by altering the fuel supply to skeletal muscle cannot be discriminated by the present study.


1990 ◽  
Vol 68 (3) ◽  
pp. 973-978 ◽  
Author(s):  
H. Rupp ◽  
R. Wahl

To define the physiological signals involved in the redirection of myosin expression in the swim-exercised rat, the relative influence of thyroid hormones and beta-adrenergic blockade was determined. Swimming exercise resulted in an increased proportion of myosin V1 (60.9 +/- 9.7 vs. 38.0 +/- 4.1% of sedentary rats fed ad libitum) but did not increase serum concentrations of total and free thyroxine or triiodothyronine determined either 17-21 h or immediately after swimming. The proportion of V1 increased, although intermittently food-deprived rats with the body weight of swimming rats exhibited a reduced proportion of V1 (23.5 +/- 2.7). When swimming rats had only intermittent access to food, they had reduced concentrations of all thyroid hormones, but the proportion of V1 (51.5 +/- 7.6) was nonetheless increased. Thus the redirection of myosin expression cannot be attributed to an increased secretion of thyroid hormones. The influence of the adrenergic system was assessed by treating swimming rats with the beta-blocking drug atenolol. Because the proportion of V1 was reduced, but thyroid hormones were not affected, beta-adrenergic blockade seems to influence myosin expression independently of thyroid hormones.


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