Steroid hormones interrelationships in the metabolic syndrome: An introduction to the ponderostat hypothesis

Alemany, M

doi:10.14310/horm.2002.1356

Cited by 16 publications

(15 citation statements)

References 277 publications

(83 reference statements)

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“…It has been proposed that glucocorticoid levels are elevated to counter inflammation in obesity and metabolic dysfunction resulting in insulin resistance, altered lipid metabolism, favored fat deposition, and protein mobilization. Estrogens may limit these actions of glucocorticoids and the inflammatory stimuli that lead to their elevation and fluctuations in estrogen levels during the life cycle can determine susceptibility to metabolic disorders [87, 88]. …”

Section: Estrogen Signaling In Metabolic Inflammationmentioning

confidence: 99%

“…Men and postmenopausal women, whose estrogen levels are low, have increased metabolic risk translated into a higher likelihood to develop cardiovascular diseases, type 2 diabetes, and certain forms of cancer [99]. The increase in cardiometabolic risk after menopause is paralleled by the redistribution of body fat and is reversed or decreased by hormone replacement therapy (HRT) [50, 88, 100]. Frequently, several altered metabolic markers are clustered in the same individual justifying the increased risk.…”

Section: Estrogen Signaling In Metabolic Inflammationmentioning

confidence: 99%

“…Regarding proinflammatory cytokines, visceral AT is associated with higher production of TNFalpha [106, 115], plasminogen activator inhibitor 1 (PAI1) [116], IL6, and CRP [117], while producing lower amounts of the anti-inflammatory, insulin-sensitizing adipokine adiponectin, which correlates more strongly with subcutaneous fat [118]. Currently, there is the suggestion that subcutaneous fat depots are protective [50, 88] and that the lack of AT, as evident in lipodystrophy [119], may equally lead to the development of metabolic syndrome.…”

Section: Estrogen Signaling In Metabolic Inflammationmentioning

confidence: 99%

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Estrogen Signaling in Metabolic Inflammation

Monteiro

Teixeira

Calhau

2014

Mediators of Inflammation

152

122

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There is extensive evidence supporting the interference of inflammatory activation with metabolism. Obesity, mainly visceral obesity, is associated with a low-grade inflammatory state, triggered by metabolic surplus where specialized metabolic cells such as adipocytes activate cellular stress initiating and sustaining the inflammatory program. The increasing prevalence of obesity, resulting in increased cardiometabolic risk and precipitating illness such as cardiovascular disease, type 2 diabetes, fatty liver, cirrhosis, and certain types of cancer, constitutes a good example of this association. The metabolic actions of estrogens have been studied extensively and there is also accumulating evidence that estrogens influence immune processes. However, the connection between these two fields of estrogen actions has been underacknowledged since little attention has been drawn towards the possible action of estrogens on the modulation of metabolism through their anti-inflammatory properties. In the present paper, we summarize knowledge on the modification inflammatory processes by estrogens with impact on metabolism and highlight major research questions on the field. Understanding the regulation of metabolic inflammation by estrogens may provide the basis for the development of therapeutic strategies to the management of metabolic dysfunctions.

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Section: Estrogen Signaling In Metabolic Inflammationmentioning

confidence: 99%

Section: Estrogen Signaling In Metabolic Inflammationmentioning

confidence: 99%

Section: Estrogen Signaling In Metabolic Inflammationmentioning

confidence: 99%

See 1 more Smart Citation

Estrogen Signaling in Metabolic Inflammation

Monteiro

Teixeira

Calhau

2014

Mediators of Inflammation

152

122

View full text Add to dashboard Cite

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“…The mechanisms of the ponderostat are still poorly understood, but probably do not depend directly on energy supply. The regulation represents a very complex process, which is influenced partly by the immune system (79). The hormones leptin and oleoyl-estrone were postulated as ponderostat signals.…”

Section: Pathophysiology Of Metabolic Syndromementioning

confidence: 99%

“…The hormones leptin and oleoyl-estrone were postulated as ponderostat signals. As the secretion capacity of leptin differs within different fat depots depending on the age, gender, and circadian rhythm, the likelihood that leptin represents a true ponderostat signal is low (79, 80, 81, 82). Recent studies have demonstrated that oleoyl-estrone itself cannot be responsible for the control of body fat, but a derivate might (83).…”

Section: Pathophysiology Of Metabolic Syndromementioning

confidence: 99%

Metabolic syndrome: is equine disease comparable to what we know in humans?

Ertelt¹,

Barton²,

Schmitz³

et al. 2014

Endocrine Connections

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This review summarizes similarities and differences between the metabolic syndromes in humans and equines, concerning the anatomy, symptoms, and pathophysiological mechanisms. In particular, it discusses the structure and distribution of adipose tissue and its specific metabolic pathways. Furthermore, this article provides insights and focuses on issues concerning laminitis in horses and cardiovascular diseases in humans, as well as their overlap.

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LPCN 1144 Resolves NAFLD in Hypogonadal Males

et al. 2020

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Hypogonadism affects hepatic lipid metabolism and is expected to promote nonalcoholic fatty liver disease (NAFLD). The aims of this study were to determine (1) the prevalence of NAFLD in hypogonadal males and (2) the impact of correction of hypogonadism by LPCN 1144 (Lipocine, Inc., Salt Lake City, UT), an oral testosterone prodrug, on NAFLD in this population. Data were derived from a multicenter open-label single-arm trial of LPCN 1144 for hypogonadal males, in which a subset (n = 36) had serial magnetic resonance imaging-proton density fat fraction measurements (National Clinical Trial 03868059). NAFLD prevalence, defined by magnetic resonance imaging-proton density fat fraction ≥5%, was 66%. Eighty-one percent of those with baseline liver fat (BL) ≥5% had improvement in liver fat content, and NAFLD resolved in 33% of subjects at 8 weeks (mean relative reduction: 45%) and 48% (mean relative reduction: 55%) after 16 weeks of LPCN 1144 therapy. The reduction in liver fat was greater in those with higher BL (BL ≥5%: 71%; BL ≥8%: 80%; and BL ≥10%: 75%). Normalization rate of alanine aminotransferase and gamma-glutamyltransferase greater than the upper limit of normal range were 100% and 50% of treated patients, respectively. LPCN 1144 was not associated with major adverse events. Conclusion: Treatment with LPCN 1144 (oral T prodrug) in hypogonadal males with NAFLD resolved NAFLD in approximately half of the affected patients without any safety signals. Further studies are needed to validate its use in hypogonadal males with nonalcoholic steatohepatitis. (Hepatology Communications 2020;4:1430-1440). T he clinical and histological spectrum of nonalcoholic fatty liver disease (NAFLD) ranges from steatosis to nonalcoholic steatohepatitis (NASH) and fibrosis, and eventually to cirrhosis. (1) The prevalence of NAFLD is rising rapidly and is now recognized as a leading indication for liver transplantation worldwide. (2) NAFLD is linked with visceral fat accumulation and metabolic syndrome, (3,4) and is associated with increased risk of cardiovascular disease and mortality. (5) Obesity, type 2 diabetes, and dyslipidemia are the main metabolic risk factors for NAFLD. (6) There are several lines of evidence suggesting a potential role of sex hormones in the genesis and

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Steroid hormones interrelationships in the metabolic syndrome: An introduction to the ponderostat hypothesis

Cited by 16 publications

References 277 publications

Estrogen Signaling in Metabolic Inflammation

Estrogen Signaling in Metabolic Inflammation

Metabolic syndrome: is equine disease comparable to what we know in humans?

LPCN 1144 Resolves NAFLD in Hypogonadal Males

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