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      Persistent Renin‐Angiotensin System Sensitization Months After Body Weight Recovery From Severe Food Restriction in Female Fischer Rats

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          Prior exposure to periods of severe food restriction (sFR) is associated with increased risk of developing hypertension and cardiovascular disease later in life.

          Methods and Results

          To investigate the mechanism of these long‐term adverse effects of sFR, 4‐month‐old female Fischer rats were divided in 2 groups and maintained on a normal diet ad libitum (control) or on an sFR diet with 60% reduction in daily food intake for 2 weeks that resulted in a 15% reduction in body weight. After the 2‐week sFR period ended, both groups received normal chow ad libitum for 3 months. Within 2 weeks after refeeding was initiated in the sFR group, body weight was restored to control levels; however, plasma angiotensinogen (1.3‐fold; P<0.05), Ang‐[1‐8] (2.0‐fold; P<0.05), and angiotensin‐converting enzyme activity (1.1‐fold; P<0.01) were all elevated 3 months after refeeding. Angiotensin type 1 receptor activity was also increased as evidenced by augmented pressor responses to angiotensin‐[1‐8] ( P<0.01) and depressor responses to the angiotensin type 1 receptor antagonist, losartan ( P<0.01) in the sFR group.


          These results indicate that sensitization of the renin‐angiotensin system persisted months after the sFR period ended. These findings may have implications for women who voluntarily or involuntarily experience an extended period of sFR and thus may be at increased risk of developing cardiovascular disease through sensitization of the renin‐angiotensin system even though their body weight, mean arterial pressure, and heart rate appear normal.

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          Most cited references 28

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          Dieting and weight cycling as risk factors for cardiometabolic diseases: who is really at risk?

          Despite the poor prognosis of dieting in obesity management, which often results in repeated attempts at weight loss and hence weight cycling, the prevalence of dieting has increased continuously in the past decades in parallel to the steadily increasing prevalence of obesity. However, dieting and weight cycling are not limited to those who are obese or overweight as substantial proportions of the various population groups with normal body weight also attempt to lose weight. These include young and older adults as well as children and adolescents who perceive themselves as too fat (due to media, parental and social pressures), athletes in weight-sensitive competitive sports (i.e. mandatory weight categories, gravitational and aesthetic sports) or among performers for whom a slim image is professionally an advantage. Of particular concern is the emergence of evidence that some of the potentially negative health consequences of repeated dieting and weight cycling are more readily seen in people of normal body weight rather than in those who are overweight or obese. In particular, several metabolic and cardiovascular risk factors associated with weight cycling in normal-weight individuals have been identified from cross-sectional and prospective studies as well as from studies of experimentally induced weight cycling. In addition, findings from studies of experimental weight cycling have reinforced the notion that fluctuations of cardiovascular risk variables (such as blood pressure, heart rate, sympathetic activity, blood glucose, lipids and insulin) with probable repeated overshoots above normal values during periods of weight regain put an additional stress on the cardiovascular system. As the prevalence of diet-induced weight cycling is increasing due to the opposing forces of an 'obesigenic' environment and the media pressure for a slim figure (that even targets children), dieting and weight cycling is likely to become an increasingly serious public health issue.
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            Cardiovascular complications of eating disorders.

            Eating disorders (anorexia nervosa and bulimia) are associated with the highest mortality rate of any psychiatric disorder. Much of this mortality and morbidity stem from cardiovascular complications such as arrhythmia related to a prolonged QTc interval and/or electrolyte disorders, hypotension, and bradycardia. Structurally, the heart in patients with eating disorders is atrophic, which may relate to longstanding hypovolemia. These patients have low cardiac output and demonstrate increased peripheral vascular resistance despite the presence of hypotension. The treatment of eating disorders is incremental caloric feeding, which can have its own intrinsic cardiovascular risk (refeeding syndrome) manifested by arrhythmia, tachycardia, congestive heart failure, and sudden cardiac death. Patients will require close monitoring and slower refeedings to minimize the risk of these complications.
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              Neurobiology and consequences of social isolation stress in animal model—A comprehensive review


                Author and article information

                J Am Heart Assoc
                J Am Heart Assoc
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                17 July 2020
                21 July 2020
                : 9
                : 14 ( doiID: 10.1002/jah3.v9.14 )
                [ 1 ] Department of Medicine Georgetown University Washington DC
                Author notes
                [* ] Correspondence to: Crystal A. West, PhD, Department of Medicine, Georgetown University, Building D, Room 396, 4000 Reservoir Road, NW, Washington, DC 20057. E-mail: caw240@

                © 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                Page count
                Figures: 8, Tables: 1, Pages: 12, Words: 7106
                Funded by: American Heart Association , open-funder-registry 10.13039/100000968;
                Award ID: 19POST34380744
                Funded by: NIH , open-funder-registry 10.13039/100000002;
                Award ID: UL1‐TR001409
                Award ID: R01‐HL119380
                Funded by: American Society of Nephrology: Carl W. Gottschalk Research Scholar Grant
                Original Research
                Original Research
                Custom metadata
                21 July 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.8 mode:remove_FC converted:29.08.2020


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