Drug treatment and obesity

Douglas, Janice G.; Munro, James

doi:10.1016/0163-7258(82)90037-7

Cited by 34 publications

(9 citation statements)

References 83 publications

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“…These drugs reduced food intake, so they were tested for their weight loss effects (44)(45)(46)(47). There is a long list of other drugs that have been used to reduce obesity including dinitrophenol, phentermine, diethylpropion, phendimetrazine, phenylpropanolamine, rainbow pills (mixture of digitalis, amphetamine and diuretics), topiramate, zonisamide, bupropion, lorcaserin, fluoxetine, atomoxetine and mazindol, and combinations such as fenfluramine-phentermine and topiramatephentermine (43,48). Further, thyroid hormones and inhibitors of gut enzymes such as α-glucosidase, α-amylase and sucrase have been used to increase the loss of fat through increased metabolic rate or through decreased absorption of nutrients from the gut, respectively (48).…”

Section: Treatment Strategies For Obesity As the Major Sign Of Metabomentioning

confidence: 99%

Functional foods as potential therapeutic options for metabolic syndrome

2015

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Obesity as part of metabolic syndrome is a major lifestyle disorder throughout the world. Current drug treatments for obesity produce small and usually unsustainable decreases in body weight with the risk of major adverse effects. Surgery has been the only treatment producing successful long-term weight loss. As a different but complementary approach, lifestyle modification including the use of functional foods could produce a reliable decrease in obesity with decreased comorbidities. Functional foods may include fruits such as berries, vegetables, fibre-enriched grains and beverages such as tea and coffee. Although health improvements continue to be reported for these functional foods in rodent studies, further evidence showing the translation of these results into humans is required. Thus, the concept that these fruits and vegetables will act as functional foods in humans to reduce obesity and thereby improve health remains intuitive and possible rather than proven.

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Section: Treatment Strategies For Obesity As the Major Sign Of Metabomentioning

confidence: 99%

Functional foods as potential therapeutic options for metabolic syndrome

2015

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“…Fenfluramine is regularly used in adult humans as an anorectic agent in the treatment of obesity (Douglas and Munro, 1982;Rowland and Carlton, 1986) and experimentally in children as a possible treatment for autism (August et al, 1984;Campbell, 1988). Thus, it is not surprising that the possibility that fenfluramine may have neurotoxic effects has led to concern over the safety of its continuing clinical use (Barnes, 1989).…”

Section: Effects Of Fenfluramine Treatment On [3hlmazindol Labelingmentioning

confidence: 99%

Effects of high‐dose fenfluramine treatment on monoamine uptake sites in rat brain: Assessment using quantitative autoradiography

Appel¹,

Mitchell²,

Contrera

et al. 1990

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Fenfluramine is an amphetamine derivative that in humans is used primarily as an anorectic agent in the treatment of obesity. In rats, subchronic high-dose d,l-fenfluramine treatment (24 mg/kg subcutaneously, twice daily for 4 days) causes long-lasting decreases in brain serotonin (5HT), its metabolite 5-hydroxyindoleacetic acid, and high-affinity 5HT uptake sites. Moreover, this high-dose treatment regimen causes both selective long-lasting decreases in fine-caliber 5HT-immunoreactive axons and appearance of other 5HT-immunoreactive axons with morphology characteristic of degenerating axons. Determination of the potential neurotoxic effects of fenfluramine treatment using immunohistochemistry is limited from the perspectives that staining is difficult to quantify and that it relies on presence of the antigen (in this case 5HT), and the 5HT-depleting effects of fenfluramine are well known. In the present study, we used quantitative in vitro autoradiography to assess, in detail, the density and regional distribution of [3H]paroxetine-labeled 5HT and [3H]mazindol-labeled catecholamine uptake sites in response to the high-dose fenfluramine treatment described above. Because monoamine uptake sites are concentrated on monoamine-containing nerve terminals, decreases in uptake site density would provide a quantitative assessment of potential neurotoxicity resulting from this fenfluramine treatment regimen. Marked decreases in densities of [3H]paroxetine-labeled 5HT uptake sites occurred in brain regions in which fenfluramine treatment decreased the density of 5HT-like immunostaining when compared to saline-treated control rats. These included cerebral cortex, caudate putamen, hippocampus, thalamus, and medial hypothalamus. Smaller, but nonetheless significant, decreases in density of [3H]paroxetine-labeled 5HT uptake sites were noted in brain regions in which partial sparing of 5HT-like immunoreactive fibers had been reported following fenfluramine treatment, specifically septum, lateral hypothalamus, and amygdala. In contrast, [3H]mazindol autoradiography revealed that total catecholamine (i.e., dopamine and norepinephrine) uptake sites in cerebral cortex, caudate putamen, and locus coeruleus, areas in which [3H]paroxetine-labeled 5HT uptake sites were significantly decreased, were unaffected by this fenfluramine treatment. These data support the hypothesis that subchronic, high-dose fenfluramine treatment causes selective degeneration of 5HT axons in rat brain. Since pharmacokinetic studies show that the dosing regimen used in this study exposes rat brain to concentrations of fenfluramine that are approximately 600 times greater than those resulting from the therapeutic oral dose, caution must be exercised in extrapolating these data to humans.

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“…In addition, induction of dietary obesity in genetically lean SHR by high-fat feeding largely prevents the rise of blood pressure in SHR (34). To complete this seeming paradox, sympathomimetic drugs used as anorectic agents for weight loss elevate blood pressure (8), whereas sympatholytic drugs used as antihypertensive agents may promote weight gain as a significant side effect (2).…”

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confidence: 99%

Refeeding hypertension in dietary obesity

Ernsberger

Nelson

1988

American Journal of Physiology-Regulatory, Integrative and Comp

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A novel model of nutritionally induced hypertension in the rat is described. Dietary obesity was produced by providing sweet milk in addition to regular chow, which elicited a 52% increase in caloric intake. Despite 54% greater body weight gain and 139% heavier retroperitoneal fat pads, 120 days of overfeeding failed to increase systolic pressure in the conscious state (125 +/- 8 vs. 121 +/- 4 mmHg in chow-fed controls) or mean arterial pressure under urethan anesthesia (71 +/- 4 vs. 63 +/- 3 mmHg). In contrast, mild hypertension developed in intermittantly fasted obese animals (a 21-mmHg increase in systolic blood pressure measured in the conscious state and a 16-mmHg increase in mean arterial pressure under anesthesia relative to chow-fed controls). The first 4-day supplemented fast was initiated 4 wk after the introduction of sweet milk, when the animals were 47 g overweight relative to chow-fed controls. Thereafter, 4 days of starvation were alternated with 2 wk of refeeding for a total of 4 cycles. A rapid fall in systolic blood pressure (12 +/- 2 mmHg at 2 days) accompanied the onset of supplemented fasting and was maintained thereafter (2.7 +/- 2.6 mmHg further decrease during the latter half of the fast). With refeeding, blood pressure rose precipitously (13 +/- 3 mmHg in the 1st 2 days), despite poststarvation anorexia. Blood pressure tended to rise slightly over the remainder of the realimentation period (5.2 +/- 2.8 mmHg). After the 4th supplemented fast, hypertension was sustained during 30 days of refeeding. Cumulative caloric intake in starved-refed rats fell within 2% of that in chow-fed controls.(ABSTRACT TRUNCATED AT 250 WORDS)

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Drug treatment and obesity

Cited by 34 publications

References 83 publications

Functional foods as potential therapeutic options for metabolic syndrome

Functional foods as potential therapeutic options for metabolic syndrome

Effects of high‐dose fenfluramine treatment on monoamine uptake sites in rat brain: Assessment using quantitative autoradiography

Refeeding hypertension in dietary obesity

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