The DOI matches its Crossref record; 120 of the 120 references it cites were found in a registry or an index; 11 of the 124 sources its claims cite were checked for support.
Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis
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TL;DR
This review synthesizes recent progress on mechanisms linking obesity and hypertension, emphasizing sympathetic overactivity, brain melanocortin/leptin/insulin pathways, adipose tissue factors, renal sodium retention, and vascular alterations. It concludes that neurogenic mechanisms are central and that better therapies require dissociating energy homeostasis from blood pressure control.
Key findings
- Obesity-associated hypertension involves excessive sympathetic nerve activity: high-fat feeding in rabbits rapidly elevated renal sympathetic tone, blood pressure, and heart rate and impaired baroreflex function as soon as 1 week after diet onset, sustained after 3 weeks; rats showed increased lumbar sympathetic activity across the entire 24-hour period, primarily via increased burst amplitude rather than burst frequency.
- The brain melanocortin system is implicated: MC4R loss-of-function mutations protected patients from obesity-associated elevations in blood pressure, heart rate, and sympathetic tone, whereas MC4R stimulation caused dose-dependent blood pressure increases in healthy overweight or obese subjects; leptin’s intravenous bolus in young healthy man increased muscle sympathetic nerve activity for over 2 hours.
- Adipose tissue contributes through paracrine/endocrine and afferent mechanisms: adipocyte-derived aldosterone and angiotensinogen are linked to vascular and blood pressure effects; adipose-specific angiotensinogen deletion protected mice from high-fat-diet hypertension without altering weight gain; leptin receptor antagonist injected into fat depots in obese rats rapidly decreased renal sympathetic activity and arterial pressure for about 15 minutes.
- Renal and vascular mechanisms are involved: renal denervation abolished hypertension in obese dogs independently of body weight but did not correct glomerular hyperfiltration; in the blinded, sham-controlled SYMPLICITY HTN-3 trial, renal denervation’s blood pressure-lowering effect after 6 months was not significantly different from sham. Vascular alterations such as arterial stiffness and endothelial dysfunction can precede hypertension and be reversed by weight loss, but are not universally associated with obesity.
Methods
- Narrative review; no primary experimental data are reported.
- Synthesizes clinical, animal, and human studies on mechanisms of obesity-associated hypertension, including radiotelemetry, microneurography, renal denervation, genetic mouse models, and adipose tissue studies.
- Main analysis is qualitative synthesis of selected literature rather than systematic review or meta-analysis.
Limitations
- The paper states that many important issues remain unaddressed: studies must dissociate energy homeostasis from blood pressure and vasomotor sympathetic control; there are still no specific guidelines for treating hypertension in obesity; clinical trials are needed; and pharmacogenomics should be integrated into personalized treatment.
- The paper notes inconsistencies in renal denervation efficacy between studies, including the disappointing SYMPLICITY HTN-3 results.
- Evident from the text: as a narrative review, it lacks a systematic search strategy, explicit inclusion criteria, formal risk-of-bias assessment, and quantitative synthesis.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
74 Not checked yet · 12 Own interpretation · 4 Supported · 3 No basis given · 2 Partly supported · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“Rats fed high fat diet also exhibited a rapid increase in radiotelemetric lumbar sympathetic activity which progresses with time, in parallel with hemodynamic and metabolic changes (21).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Excessive sympathetic nerve activity
What the sources say
- Supportedcites [21] Muntzel MS Al-Naimi OA Barclay A Ajasin D Cafeteria diet increases fat mass and chronically elevates lumbar sympathetic nerve activity in rats Hypertension 2012 60 1498 1502 23090774 PMC3535318 source
The Results report that lumbar sympathetic nerve activity in cafeteria-fed female Wistar rats increased over time and became significantly elevated by day 12. The study used radiotelemetry and also found higher overall heart rates and increased fat mass and leptin. Its Discussion notes that mean arterial pressure was not clearly elevated, but the claim does not specifically assert a blood-pressure increase. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Given that excessive sympathetic activity is common in obesity, β-blockers appear as an obvious pharmacologic therapy to treat the hypertension associated with this condition, but treatment with β-blockers leads to metabolic complications including weight gain (16–18).”
What the sources say
- Supportedcites [16] Julius S Valentini M Palatini P Overweight and hypertension - A 2-way street? Hypertension 2000 35 807 813 10720599 source
The “Data That Support the Hypothesis” section reports weight gain during both short- and long-term β-blocker therapy, including a significant increase in β-blocker-treated patients in the HAPPHY trial. It also describes reduced thermogenesis as a possible mechanism. Page numbers were not supplied in our copy. (LLM, conf=0.92)
- Partly supportedcites [17] Zhou X Ma L Habibi J Whaley-Connell A Hayden MR Tilmon RD Brown AN Kim JA Demarco VG Sowers JR Nebivolol improves diastolic dysfunction and myocardial remodeling through reductions in oxidative stress in the Zucker obese rat Hypertension 2010 55 880 888 20176997 PMC2841702 sourceExperimental — accuracy not yet measured
The Introduction says traditional β-blockers have been associated with weight gain and worsening insulin resistance. But it distinguishes nebivolol, which it says does not cause weight gain or adversely affect insulin resistance; the Discussion reports reduced weight gain in nebivolol-treated rats. The claim overgeneralizes this complication to β-blockers as a class. (LLM, conf=0.88)
- Not checked yetcites [18] Jordan J Engeli S Boschmann M Weidinger G Luft FC Sharma AM Kreuzberg U Hemodynamic and metabolic responses to valsartan and atenolol in obese hypertensive patients J Hypertens 2005 23 2313 2318 16269974 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Disruption of leptin receptor signaling in POMC neurons abolished the ability of exogenous leptin administration to increase blood pressure (39;41) which provides additional support to the notion that leptin is a critical hormone in coupling hypertension and obesity (Figure 1).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Brain mechanisms
What the sources say
- Supportedcites [39] do Carmo JM da Silva AA Cai ZW Lin SY Dubinion JH Hall JE Control of Blood Pressure, Appetite, and Glucose by Leptin in Mice Lacking Leptin Receptors in Proopiomelanocortin Neurons Hypertension 2011 57 918 926 21422382 PMC3092393 source
The Discussion states that deleting leptin receptors in POMC neurons abolished leptin’s chronic effect on mean arterial pressure in mice. It also reports that chronic leptin infusion raised blood pressure in control mice but not in mice lacking those receptors. (LLM, conf=0.94)
- Supportedcites [41] Dubinion JH do Carmo JM Adi A Hamza S da Silva AA Hall JE Role of proopiomelanocortin neuron Stat3 in regulating arterial pressure and mediating the chronic effects of leptin Hypertension 2013 61 1066 1074 23529161 PMC3678380 source
The Results section reports that seven days of leptin infusion raised blood pressure in control mice but produced no significant increase in mice lacking Stat3 signaling in POMC neurons. The Discussion likewise states that POMC-neuron Stat3 inactivation abolished the blood-pressure rise during chronic leptin treatment. The experiment disrupted this downstream signaling pathway, rather than deleting the leptin receptor itself. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Obesity is associated with several other changes in the kidney that promote the development of hypertension as well as chronic kidney disease and end-stage renal disease.”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Renal mechanisms
What the sources say
- Partly supportedcites [63] Foster MC Hwang SJ Porter SA Massaro JM Hoffmann U Fox CS Fatty kidney, hypertension, and chronic kidney disease: the Framingham Heart Study Hypertension 2011 58 784 790 21931075 PMC3204377 sourceExperimental — accuracy not yet measured
The Discussion (page not provided) describes obesity-related kidney changes and an association with hypertension and CKD. It treats the mechanisms by which those changes might contribute to disease as proposed rather than established, and our copy does not address end-stage renal disease. (LLM, conf=0.86)
- Partly supportedcites [64] Belin de Chantemele EJ Ali MI Mintz JD Rainey WE Tremblay ML Fulton DJ Stepp DW Increasing peripheral insulin sensitivity by protein tyrosine phosphatase 1B deletion improves control of blood pressure in obesity Hypertension 2012 60 1273 1279 23045458 PMC3475734 sourceExperimental — accuracy not yet measured
The Results (Renal Morphology; page not available) report structural kidney changes in obese mice. The Discussion (Potential mechanisms—Renal Injury; page not available) says kidney injury may be a result rather than a cause of impaired blood-pressure control. The paper does not establish that these changes promote hypertension, chronic kidney disease, or end-stage renal disease. (LLM, conf=0.86)
- Partly supportedcites [65] Beyer AM Raffai G Weinberg B Fredrich K Lombard JH Dahl salt-sensitive rats are protected against vascular defects related to diet-induced obesity Hypertension 2012 60 404 410 22710645 PMC3444144 sourceExperimental — accuracy not yet measured
The Introduction (page unavailable in our copy) says obesity is frequently accompanied by elevated blood pressure and renal damage. It does not say that changes in the kidney promote hypertension, nor does it address chronic kidney disease or end-stage renal disease. (LLM, conf=0.85)
- Partly supportedcites [66] Guo DF Beyer AM Yang BL Nishimura DY Sheffield VC Rahmouni K Inactivation of Bardet-Biedl syndrome genes causes kidney defects Am J Physiol Renal Physiol 2011 300 F574 F580 21106857 PMC3043995 sourceExperimental — accuracy not yet measured
The Abstract reports obesity-related kidney abnormalities in Bardet–Biedl syndrome (BBS) mouse models and says end-stage renal disease is frequent in BBS patients. But the paper does not establish that obesity-associated kidney changes promote hypertension or chronic kidney disease generally; the Discussion instead considers hypertension as a possible contributor to renal abnormalities. (LLM, conf=0.86)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This is based on the observation that female sheep are protected from adverse renal effects caused by obesity despite exhibiting similar metabolic and cardiovascular phenotypes as the male counterparts (67).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Renal mechanisms
What the sources say
- Supportedcites [67] Bloor ID Sebert SP Mahajan RP Symonds ME The influence of sex on early stage markers of kidney dysfunction in response to juvenile obesity Hypertension 2012 60 991 997 22949537 source
The Discussion (page unavailable in our copy) explicitly reports similar metabolic and cardiovascular outcomes of juvenile obesity in both sexes, but adverse kidney-cell responses only in males. The paper also concludes that young female sheep were protected from adverse renal effects of obesity. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The efficacy of chronic treatment with Ang 1–7, a peptide that negatively modulate RAS activity, in alleviating obesity-associated impairment in endothelium-dependent vasodilation supports further the pathophysiological role of the RAS in obesity-related endothelial dysfunction (73).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Vascular alterations
What the sources say
- Supportedcites [73] Beyer AM Guo DF Rahmouni K Prolonged treatment with angiotensin 1–7 improves endothelial function in diet-induced obesity J Hypertens 2013 31 4 730 738 23425706 PMC5684878 source
The Discussion states that chronic Ang 1–7 treatment improved impaired endothelium-dependent vasodilation caused by obesity. It also identifies this finding as evidence of a protective vascular role for Ang 1–7 in obesity-associated endothelial dysfunction. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Supported
In the paper
“Interestingly, sympathetic overdrive was also found to be closely related to subclinical cardiovascular and renal alterations that develop in obese subjects even in the absence of hypertension (19).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Excessive sympathetic nerve activity
What the sources say
- Not checked yetcites [19] Lambert E Sari CI Dawood T Nguyen J McGrane M Eikelis N Chopra R Wong C Chatzivlastou K Head G Straznicky N Esler M Schlaich M Lambert G Sympathetic nervous system activity is associated with obesity-induced subclinical organ damage in young adults Hypertension 2010 56 351 358 20625075 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“Moreover, obesity is a major risk factor for resistant hypertension, i.e. patients who have uncontrolled blood pressure despite being on three or more antihypertensive medications (7;8).”
What the sources say
- Not checked yetcites [7] Goodfriend TL Calhoun DA Resistant hypertension, obesity, sleep apnea, and aldosterone: theory and therapy Hypertension 2004 43 518 524 14732721 source
- Not checked yetcites [8] Persell SD Prevalence of resistant hypertension in the United States, 2003–2008 Hypertension 2011 57 1076 1080 21502568 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“Clinical and animal studies have documented that weight gain can raise arterial pressure whereas weight loss has a beneficial effect on blood pressure control (9–11).”
What the sources say
- Not checked yetcites [9] De CC Porteri E Rizzoni D Corbellini C La BE Boari GE Pilu A Mittempergher F Di BE Casella C Nascimbeni R Rosei CA Ruggeri G Caimi L Rosei EA Effects of weight loss on structural and functional alterations of subcutaneous small arteries in obese patients Hypertension 2011 58 29 36 21555677 source
- Not checked yetcites [10] Haufe S Utz W Engeli S Kast P Bohnke J Pofahl M Traber J Haas V Hermsdorf M Mahler A Busjahn A Wiesner S Otto C Mehling H Luft FC Boschmann M Schulz-Menger J Jordan J Left ventricular mass and function with reduced-fat or reduced-carbohydrate hypocaloric diets in overweight and obese subjects Hypertension 2012 59 70 75 22068866 source
- Not checked yetcites [11] Weisbrod RM Shiang T Al SL Fry JL Bajpai S Reinhart-King CA Lob HE Santhanam L Mitchell G Cohen RA Seta F Arterial stiffening precedes systolic hypertension in diet-induced obesity Hypertension 2013 62 1105 1110 24060894 PMC3951434 source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“The close relationship between excess adipose mass and hypertension is well documented, with population-based studies showing excess adiposity as the strongest known risk factor for hypertension in male and female subjects of different ages and races (1–5).”
What the sources say
- Not checked yetcites [1] Jones A Charakida M Falaschetti E Hingorani AD Finer N Masi S Donald AE Lawlor DA Smith GD Deanfield JE Adipose and height growth through childhood and blood pressure status in a large prospective cohort study Hypertension 2012 59 919 925 22493074 PMC3428923 source
- Not checked yetcites [2] Suglia SF Clark CJ Gary-Webb TL Adolescent obesity, change in weight status, and hypertension: racial/ethnic variations Hypertension 2013 61 290 295 23248147 PMC3938160 source
- Not checked yetcites [3] Tu W Eckert GJ DiMeglio LA Yu Z Jung J Pratt JH Intensified effect of adiposity on blood pressure in overweight and obese children Hypertension 2011 58 818 824 21968752 PMC3433397 source
- Not checked yetcites [4] Selassie A Wagner CS Laken ML Ferguson ML Ferdinand KC Egan BM Progression is accelerated from prehypertension to hypertension in blacks Hypertension 2011 58 579 587 21911708 PMC3186683 source
- Not checked yetcites [5] Pausova Z Mahboubi A Abrahamowicz M Leonard GT Perron M Richer L Veillette S Gaudet D Paus T Sex differences in the contributions of visceral and total body fat to blood pressure in adolescence Hypertension 2012 59 572 579 22291448 source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 18
- Probably not a substantial claim. 1
In the paper
“Indeed, these changes appeared as soon a 1 week after starting the high fat diet and sustained after 3 weeks (20).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Excessive sympathetic nerve activity
What the sources say
- Not checked yetcites [20] Armitage JA Burke SL Prior LJ Barzel B Eikelis N Lim K Head GA Rapid onset of renal sympathetic nerve activation in rabbits fed a high-fat diet Hypertension 2012 60 163 171 22647890 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Activation of the sympathetic nervous system which is a common feature of obesity is widely recognized as a major contributor to the development and maintenance of hypertension.”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Excessive sympathetic nerve activity
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“At first glance, this recommendation seems compelling, but evidence suggests that weight loss through lifestyle modifications for obesity-associated hypertension is neither simple nor sustained and is also not consistently effective as antihypertensive therapy (15).”
What the sources say
- Not checked yetcites [15] Mark AL Dietary therapy for obesity: An emperor with no clothes Hypertension 2008 51 1426 1433 18474832
hedged- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Rabbits instrumented for telemetric recording of renal sympathetic activity and hemodynamic measurements were found to develop a rapid elevation in renal sympathetic tone, blood pressure and heart rate and impairment in baroreflex function when fed a high fat diet (20).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Excessive sympathetic nerve activity
What the sources say
- Not checked yetcites [20] Armitage JA Burke SL Prior LJ Barzel B Eikelis N Lim K Head GA Rapid onset of renal sympathetic nerve activation in rabbits fed a high-fat diet Hypertension 2012 60 163 171 22647890 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In this regard, accumulating evidence suggests that genetic variants may impact the sensitivity to weight loss as well as blood pressure response to weight change.”
What the sources say
- Not checked yetcites [12] Zhang X Qi Q Liang J Hu FB Sacks FM Qi L Neuropeptide Y promoter polymorphism modifies effects of a weight-loss diet on 2-year changes of blood pressure: the preventing overweight using novel dietary strategies trial Hypertension 2012 60 1169 1175 22966009 PMC3869086
- Not checked yetcites [13] Kostis WJ Cabrera J Hooper WC Whelton PK Espeland MA Cosgrove NM Cheng JQ Deng Y De SC Pyle M Maruthur N Reyes I Anderson CA Liu J Kostis JB Relationships between selected gene polymorphisms and blood pressure sensitivity to weight loss in elderly persons with hypertension Hypertension 2013 61 857 863 23438931 PMC4636329
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Further analysis revealed that high fat feeding in rats increased lumbar sympathetic discharge during the entire 24-hour period and this increase was primarily caused by a rise in burst amplitude and not through changes in burst frequency (21), indicating an increasing number of recruited nerve fibers.”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Excessive sympathetic nerve activity
What the sources say
- Not checked yetcites [21] Muntzel MS Al-Naimi OA Barclay A Ajasin D Cafeteria diet increases fat mass and chronically elevates lumbar sympathetic nerve activity in rats Hypertension 2012 60 1498 1502 23090774 PMC3535318
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The melanocortin system has a powerful influence on energy homeostasis and is critically involved in mediating the metabolic, sympathetic and cardiovascular effects of leptin and insulin (32–35).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Brain mechanisms
What the sources say
- Not checked yetcites [32] Hall JE da Silva AA do Carmo JM Dubinion J Hamza S Munusamy S Smith G Stec DE Obesity-induced Hypertension: Role of Sympathetic Nervous System, Leptin, and Melanocortins J Biol Chem 2010 285 17271 17276 20348094 PMC2878489 source
- Not checked yetcites [33] Harlan SM Rahmouni K Neuroanatomical determinants of the sympathetic nerve responses evoked by leptin Clin Auton Res 2013 23 1 7 22714900 PMC3496820
- Not checked yetcites [34] Carlson SH Wyss JM Mechanisms underlying hypertension and obesity: a melanocortin linkage in the brain Hypertension 2011 57 375 376 21263117
- Not checked yetcites [35] Ward KR Bardgett JF Wolfgang L Stocker SD Sympathetic response to insulin is mediated by melanocortin 3/4 receptors in the hypothalamic paraventricular nucleus Hypertension 2011 57 435 441 21263116 PMC3580160 source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The fact that several brain nuclei are implicated in the renal sympathetic nerve activation triggered by leptin is consistent with the idea that leptin action in the brain involves a distributed network.”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Brain mechanisms
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Notably, central administration of an insulin receptor antagonist to obese rabbits also decreased arterial pressure, but with no concomitant change in renal sympathetic traffic (50).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Brain mechanisms
What the sources say
- Not checked yetcites [50] Lim K Burke SL Head GA Obesity-related hypertension and the role of insulin and leptin in high-fat-fed rabbits Hypertension 2013 61 628 634 23339171 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The anti-contractile effects of perivascular adipose tissue has now been extended to peripheral skeletal muscle arteries and shown to involve the opening of a particular K+ channel (KCNQ) in smooth muscle (56).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Contribution of adipose tissue
What the sources say
- Not checked yetcites [56] Zavaritskaya O Zhuravleva N Schleifenbaum J Gloe T Devermann L Kluge R Mladenov M Frey M Gagov H Fesus G Gollasch M Schubert R Role of KCNQ channels in skeletal muscle arteries and periadventitial vascular dysfunction Hypertension 2013 61 151 159 23184384
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Interestingly, renal denervation did not lower the elevated heart rate or the plasma norepinephrine levels in the obese dogs (22).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Excessive sympathetic nerve activity
What the sources say
- Not checked yetcites [22] Lohmeier TE Iliescu R Liu B Henegar JR Maric-Bilkan C Irwin ED Systemic and renal-specific sympathoinhibition in obesity hypertension Hypertension 2012 59 331 338 22184321 PMC3277854 source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“However, these mice had unaltered body weight, food intake and brown adipose tissue sympathetic responses to leptin (42).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Brain mechanisms
What the sources say
- Not checked yetcites [42] Young CN Morgan DA Butler SD Mark AL Davisson RL The brain subfornical organ mediates leptin-induced increases in renal sympathetic activity but not its metabolic effects Hypertension 2013 61 737 744 23357182 PMC3832948
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These vascular abnormalities are thought to contribute and even predict the development of hypertension and other cardiovascular complications (9;11;64;69–71).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Vascular alterations
What the sources say
- Not checked yetcites [9] De CC Porteri E Rizzoni D Corbellini C La BE Boari GE Pilu A Mittempergher F Di BE Casella C Nascimbeni R Rosei CA Ruggeri G Caimi L Rosei EA Effects of weight loss on structural and functional alterations of subcutaneous small arteries in obese patients Hypertension 2011 58 29 36 21555677
- Not checked yetcites [11] Weisbrod RM Shiang T Al SL Fry JL Bajpai S Reinhart-King CA Lob HE Santhanam L Mitchell G Cohen RA Seta F Arterial stiffening precedes systolic hypertension in diet-induced obesity Hypertension 2013 62 1105 1110 24060894 PMC3951434
- Not checked yetcites [64] Belin de Chantemele EJ Ali MI Mintz JD Rainey WE Tremblay ML Fulton DJ Stepp DW Increasing peripheral insulin sensitivity by protein tyrosine phosphatase 1B deletion improves control of blood pressure in obesity Hypertension 2012 60 1273 1279 23045458 PMC3475734
- Not checked yetcites [69] Lurbe E Torro I Garcia-Vicent C Alvarez J Fernandez-Fornoso JA Redon J Blood pressure and obesity exert independent influences on pulse wave velocity in youth Hypertension 2012 60 550 555 22733475
- Not checked yetcites [70] Cao J Peterson SJ Sodhi K Vanella L Barbagallo I Rodella LF Schwartzman ML Abraham NG Kappas A Heme oxygenase gene targeting to adipocytes attenuates adiposity and vascular dysfunction in mice fed a high-fat diet Hypertension 2012 60 467 475 22753217 PMC3423899
- Not checked yetcites [71] Marshall NJ Liang L Bodkin J Dessapt-Baradez C Nandi M Collot-Teixeira S Smillie SJ Lalgi K Fernandes ES Gnudi L Brain SD A role for TRPV1 in influencing the onset of cardiovascular disease in obesity Hypertension 2013 61 246 252 23150506
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“For instance, improving insulin sensitivity in obese mice through Protein Tyrosine Phosphatase 1B deletion corrected the reduced albumin excretion, but not Na+ and K+ excretion nor the structural changes in the kidney (64).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Renal mechanisms
What the sources say
- Not checked yetcites [64] Belin de Chantemele EJ Ali MI Mintz JD Rainey WE Tremblay ML Fulton DJ Stepp DW Increasing peripheral insulin sensitivity by protein tyrosine phosphatase 1B deletion improves control of blood pressure in obesity Hypertension 2012 60 1273 1279 23045458 PMC3475734
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Volume expansion and sodium retention are major features of obesity.”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Renal mechanisms
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In fact, renal denervation in obese dogs led to a further increase in glomerular filtration rate whereas fractional sodium excretion remained suppressed (22).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Renal mechanisms
What the sources say
- Not checked yetcites [22] Lohmeier TE Iliescu R Liu B Henegar JR Maric-Bilkan C Irwin ED Systemic and renal-specific sympathoinhibition in obesity hypertension Hypertension 2012 59 331 338 22184321 PMC3277854 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Perhaps the most intriguing observation in this study relate to the demonstration that adipose tissue modulate blood pressure through its profound effect on Ang II synthesis, but the mechanisms involved remain to be defined (58).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Contribution of adipose tissue
What the sources say
- Not checked yetcites [58] Grobe JL Rahmouni K The adipose/circulating renin-angiotensin system cross-talk enters a new dimension Hypertension 2012 60 1389 1390 23108659 PMC3959780
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Selective ablation of adipose tissue angiotensinogen did not alter the weight gain and other metabolic changes caused by high fat diet, but it protected mice from hypertension (57).”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Contribution of adipose tissue
What the sources say
- Not checked yetcites [57] Yiannikouris F Gupte M Putnam K Thatcher S Charnigo R Rateri DL Daugherty A Cassis LA Adipocyte deficiency of angiotensinogen prevents obesity-induced hypertension in male mice Hypertension 2012 60 1524 1530 23108647 PMC3517298
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Defects in various biological processes ranging from genetic and humoral factors to basic cellular signaling pathways in different tissues have been involved in the pathogenesis of obesity-related hypertension.”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Conclusions and perspectives
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
- Rests on an assumption: The obesity epidemic is associated with an increasing prevalence of cardiovascular risk factors including hypertension.
The paper relies on this without support.
The obesity epidemic is associated with an increasing prevalence of cardiovascular risk factors including hypertension.
“The epidemic of obesity is associated with raising prevalence of cardiovascular risk factors including hypertension.”
The paper relies on this without support.
There are no specific guidelines for the treatment of hypertension in an obesity setting.
“Also, despite the wide range of available anti-hypertensive drugs there are still no specific guidelines for the treatment of hypertension in an obesity setting.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In addition to inhibiting appetite and increasing metabolism, stimulation of hypothalamic melanocortin-4 receptors increases sympathetic activity and blood pressure74,75.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [74]
Experimental — accuracy not yet measuredIn the citing paper
“Rodents with loss of function mutations in the hypothalamic melanocortin-4 receptors are obese but lack sympathetic activation and obesity-associated hypertension74,75.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [74]
In the citing paper
“The brain melanocortin pathway has emerged from studies in both experimental animals74,75 and humans89,90 as a crucial pathway in the regulation of sympathetic activity and BP in obesity.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [74]
In the citing paper
“A large body of evidence has demonstrated that leptin contributes to sympathetic overactivity and hypertension in a number of animal models of monogenic and diet-induced obesity74–77.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [74]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Renal mechanisms
“corrected the reduced albumin excretion”
§ Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis > Renal mechanisms
“This finding point to a pathological role of insulin resistance in the albuminuria associated with obesity”
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Indices of Obesity and Cardiovascular Risk Factors in British Women
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Metadata
- Authors
- Rahmouni, K.
- Affiliations
- University of Iowa (US)
- Corresponding author
- Rahmouni, Kamal
- ORCID
- Rahmouni, Kamal
- Venue
- Hypertension
- Published
- 2014-08
- Volume
- 64
- Issue
- 2
- Pages
- 215-221
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- PMC
- PMC4184930
- OpenAlex
- W2107915427
- Cited by
- 150
- References
- 120
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 6 · 2023: 7 · 2022: 2 · 2021: 9 · 2020: 9 · 2019: 12 · 2018: 13 · 2017: 19 · 2016: 16 · 2015: 20 · 2014: 2
- FWCI
- 2.97
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL-084207, P01HL084207)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- obesity, obesity-related hypertension
- MeSH terms
- Humans, Hypertension, Obesity
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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