Principles of Endocrinology

Kronenberg, Henry M.; Мелмед, Шломо; Larsen, P. Reed; Polonsky, Kenneth S.

doi:10.1016/b978-1-4377-0324-5.00001-8

Cited by 65 publications

(102 citation statements)

References 17 publications

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“…The data herein also provide support for our second hypothesis that FCF is increased in horses with endocrine disease and associated with hyperinsulinemia, with a significant, almost 2‐fold increase in FCF, but not total cortisol observed in animals with PPID as compared to healthy age‐matched horses. Free cortisol fraction was also similarly and significantly increased in horses and ponies with endocrine disease (PPID or EMS) and concurrent ID characterized by hyperinsulinemia, and FCF and insulin were significantly and positively correlated in these hyperinsulinemic animals as anticipated and as described in people 16, 17, 20, 34, 35…”

Section: Discussionsupporting

confidence: 54%

“…Cortisol is an important glucose counter‐regulatory hormone that increases blood glucose; specifically, corticosteroids antagonize the effects of insulin by stimulating hepatic gluconeogenesis and by inhibiting cellular glucose uptake by preventing membrane localization of GLUT‐4 glucose transporters 20, 61. This peripheral tissue insulin resistance results in persistently normal to high blood glucose concentrations, which provides continued stimulus for insulin release and eventually results in hyperinsulinemia.…”

Section: Discussionmentioning

confidence: 99%

“…This is mostly likely because of obesity‐related increases in HPA axis activity or 11‐β‐HSD1 expression,48, 49, 50, 51, 52, 53, 54, 55 as discussed above in relation to FCF in animals with endocrine disease. It is possible that an increase in total circulating cortisol, which has global anti‐inflammatory effects that include inhibition of pro‐inflammatory mediator production and leukocyte migration into tissues,7, 20, 63 is actually an appropriate response to an obesity‐induced inflammatory state. Alternatively, it is possible that, as discussed for FCF, circulating total cortisol excess attributable to genetic differences, environmental stress, or undiagnosed hypothalamic–pituitary–adrenal (HPA) axis dysregulation could actually be the primary factor that stimulates adipocyte proliferation and increased body fat deposition,37 and thus ultimately results in obesity in affected horses and ponies.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Age, Season, Body Condition, and Endocrine Status on Serum Free Cortisol Fraction and Insulin Concentration in Horses

Hart

Wochele

Norton

et al. 2016

Veterinary Internal Medicne

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BackgroundIncreased free cortisol fraction is associated with insulin dysregulation (ID) in people with Metabolic Syndrome and Cushing's Disease. Free cortisol has not been investigated in equine endocrine disorders.Hypotheses(1) In healthy horses, sex, age, body condition score (BCS), and season impact free cortisol; (2) free cortisol is increased in horses with Pituitary Pars Intermedia Dysfunction (PPID) or Equine Metabolic Syndrome (EMS).AnimalsFifty‐seven healthy horses; 40 horses and ponies with PPID (n = 20) or EMS (n = 20).MethodsProspective study. Serum collected seasonally from healthy animals and archived serum from PPID and EMS animals was analyzed for insulin, total and free cortisol concentrations, and free cortisol fraction (FCF). Linear mixed models were used to determine effects of age, sex, season, and BCS on hormones in controls. Hormone measurements were compared between disease groups and age‐ and season‐matched controls with t‐tests. EMS and hyperinsulinemic PPID animals were combined in an ID (hyperinsulinemia) group.ResultsFree cortisol concentrations were increased in overweight/obese controls (0.3 ± 0.1 μg/dL) compared to lean controls (0.2 ± 0.1 μg/dL; P = .017). Mean FCF was significantly higher in animals with PPID (8.8 ± 5.8 μg/dL, P = .005) or ID (8.8 ± 10.2 μg/dL, P = .039) than controls (5.0 ± 0.9 μg/dL), but total cortisol concentrations were similar (P ≥ .350) (PPID: 4.2 ± 4.3 μg/dL; ID: 5.0 ± 4.5 μg/dL; controls: 4.6 ± 1.7 and 5.1 ± 2.1 μg/dL).Conclusions and Clinical ImportanceIncreased FCF is associated with obesity in healthy horses and with ID (hyperinsulinemia) in horses and ponies with endocrine disease. Decreased plasma cortisol‐binding capacity could be a component of these endocrine disorders in horses.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of Age, Season, Body Condition, and Endocrine Status on Serum Free Cortisol Fraction and Insulin Concentration in Horses

Hart

Wochele

Norton

et al. 2016

Veterinary Internal Medicne

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“…The mammalian hypothalamus regulates essential and dynamic physiological functions, including growth, metabolism, sleep, as well as reproductive behaviors (Krononberg et al, 2007;Caqueret et al, 2005;Michaud, 2001). The hypothalamus comprises of complex networked sets of nuclei that regulate homeostatic function through production and delivery of neuropeptide to distinct targets (Swanson and Sawchenko, 1983).…”

Section: Introductionmentioning

confidence: 99%

Notch/Rbpjκ signaling regulates progenitor maintenance and differentiation of hypothalamic arcuate neurons

Aujla

Naratadam

et al. 2013

Development

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SUMMARYThe hypothalamic arcuate nucleus (Arc), containing pro-opoiomelanocortin (POMC), neuropeptide Y (NPY) and growth hormone releasing hormone (GHRH) neurons, regulates feeding, energy balance and body size. Dysregulation of this homeostatic mediator underlies diseases ranging from growth failure to obesity. Despite considerable investigation regarding the function of Arc neurons, mechanisms governing their development remain unclear. Notch signaling factors such as Hes1 and Mash1 are present in hypothalamic progenitors that give rise to Arc neurons. However, how Notch signaling controls these progenitor populations is unknown. To elucidate the role of Notch signaling in Arc development, we analyzed conditional loss-of-function mice lacking a necessary Notch co-factor, Rbpjκ, in Nkx2.1-cre-expressing cells (Rbpjκ cKO), as well as mice with expression of the constitutively active Notch1 intracellular domain (NICD) in Nkx2.1-cre-expressing cells (NICD Tg). We found that loss of Rbpjκ results in absence of Hes1 but not of Hes5 within the primordial Arc at E13.5. Additionally, Mash1 expression is increased, coincident with increased proliferation and accumulation of Arc neurons at E13.5. At E18.5, Rbpjκ cKO mice have few progenitors and show increased numbers of differentiated Pomc, NPY and Ghrh neurons. By contrast, NICD Tg mice have increased hypothalamic progenitors, show an absence of differentiated Arc neurons and aberrant glial differentiation at E18.5. Subsequently, both Rbpjκ cKO and NICD Tg mice have changes in growth and body size during postnatal development. Taken together, our results demonstrate that Notch/Rbpjκ signaling regulates the generation and differentiation of Arc neurons, which contribute to homeostatic regulation of body size. KEY WORDS: Arcuate, Notch, POMC, NPY, Hypothalamus, MouseNotch/Rbpjκ signaling regulates progenitor maintenance and differentiation of hypothalamic arcuate neurons Paven K. Aujla, George T. Naratadam, Liwen Xu and Lori T. Raetzman* DEVELOPMENT 3512During embryonic development, cells migrate from the hypothalamic ventricular zone (HVZ) surrounding the ventral region of the third ventricle in order to form the Arc by E16.5 (Bayer and Altman, 1987;Ishii and Bouret, 2012;Shimada and Nakamura, 1973). One of the major functions of the Arc is to respond to food intake and energy expenditure. Energy-related hormone signals such as leptin are sensed by anorexic proopoiomelanocortin (POMC)/cocaine and amphetamine-regulated transcript (CART) neurons and orexic neuropeptide Y (NPY)/Agouti-related peptide (AgRP) neurons. POMC and NPY neurons regulate feeding behavior and are crucial to maintaining proper energy balance and homeostasis (Broberger, 2005;Morton et al., 2006;Srinivas et al., 2001). An additional subtype of neurons, growth hormone-releasing hormone (GHRH) neurons, are present in the Arc and regulate body size and growth by controlling release of growth hormone from the pituitary gland (Bouyer et al., 2007; Grossman et al., 1986).Despite the functional importance of ...

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“…Thus, maintaining thyroid homeostasis is essential for human health. The production and secretion of thyroid hormones by the thyroid are directly regulated by the hypothalamus-pituitary-thyroid axis [12] . The pituitary gland serves as a sophisticated biosensor of thyroid hormone levels and regulates thyrotropin (TSH) levels according to the feedback of free thyroxine (FT4) and free triiodothyronine (FT3).…”

Section: Introductionmentioning

confidence: 99%

Dietary high-fat lard intake induces thyroid dysfunction and abnormal morphology in rats

et al. 2014

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Aim: Excess dietary fat intake can induce lipotoxicity in non-adipose tissues. The aim of this study was to observe the effects of dietary high-fat lard intake on thyroid in rats. Methods: Male Sprague-Dawley rats were fed a high-fat lard diet for 24 weeks, and then the rats were fed a normal control diet (acute dietary modification) or the high-fat lard diet for another 6 weeks. The serum lipid profile, total thyroxine (TT4), free thyroxine (FT4) and thyrotropin (TSH) levels were determined at the 12, 18, 24 and 30 weeks. High-frequency ultrasound scanning of the thyroid glands was performed at the 24 or 30 weeks. After the rats were sacrificed, the thyroid glands were collected for histological and immunohistochemical analyses. Results: The high-fat lard diet significantly increased triglyceride levels in both the serum and thyroid, and decreased serum TT4 and FT4 levels in parallel with elevated serum TSH levels. Ultrasonic imaging revealed enlarged thyroid glands with lowered echotexture and relatively heterogeneous features in the high-fat lard fed rats. The thyroid glands from the high-fat lard fed rats exhibited enlarged follicle cavities and flattened follicular epithelial cells under light microscopy, and dilated endoplasmic reticulum cisternae, twisted nuclei, fewer microvilli and secretory vesicles under transmission electron microscopy. Furthermore, the thyroid glands from the highfat lard fed rats showed markedly low levels of thyroid hormone synthesis-related proteins TTF-1 and NIS. Acute dietary modification by withdrawal of the high-fat lard diet for 6 weeks failed to ameliorate the high-fat lard diet-induced thyroid changes. Conclusion: Dietary high-fat lard intake induces significant thyroid dysfunction and abnormal morphology in rats, which can not be corrected by short-term dietary modification.

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Principles of Endocrinology

Cited by 65 publications

References 17 publications

Effect of Age, Season, Body Condition, and Endocrine Status on Serum Free Cortisol Fraction and Insulin Concentration in Horses

Effect of Age, Season, Body Condition, and Endocrine Status on Serum Free Cortisol Fraction and Insulin Concentration in Horses

Notch/Rbpjκ signaling regulates progenitor maintenance and differentiation of hypothalamic arcuate neurons

Dietary high-fat lard intake induces thyroid dysfunction and abnormal morphology in rats

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