Thyroid hormone’s role in regulating brain glucose metabolism and potentially modulating hippocampal cognitive processes

Jahagirdar, V.; McNay, Ewan C.

doi:10.1007/s11011-012-9291-0

Cited by 28 publications

(13 citation statements)

References 181 publications

(212 reference statements)

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“…Among the most striking clinical manifestations in patients diagnosed with NMDAR encephalitis, deficits in cognition, such as memory, and behavior are also associated with thyroid function [17,26,27]. In our findings, patients, especially those whose consciousness decreased, frequently had low T3 syndrome.…”

Section: Discussionsupporting

confidence: 49%

Thyroid Function and Autoimmune Indications in Patients with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

Ma¹,

Yin²,

Zeng³

et al. 2018

Neuroimmunomodulation

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Objective: Previous studies have shown that functional abnormalities of the thyroid are associated with the pathogenesis of several neurological diseases. However, their relationship in patients with anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis remains to be defined. Methods: Forty-three patients with anti-NMDAR encephalitis were examined for thyroid function and autoimmune indications, in comparison with 225 healthy controls (CTL). Patients were further classified into 2 subgroups based on their free tri-iodothyronine (fT3) levels. Moreover, fT3 levels were also investigated after at least three months of follow-up. The clinical characteristics of the patients and CTL were described in detail. Results: Serum levels of fT3 and thyroid-stimulating hormone (TSH) were found to be relatively lower in patients with anti-NMDAR encephalitis than in CTL (both p < 0.001). Low T3 syndrome also occurred more frequently in anti- NMDAR encephalitis (25.6 vs. 0.4%, p < 0.001). However, no statistical differences were detected between patients and CTL in terms of the positive rate of thyroid antibodies and other types of thyroid dysfunction. Patients with low T3 levels tended to have a longer hospital stay (p = 0.006), a higher rate of abnormal brain magnetic resonance imaging (MRI) findings (p = 0.033), a higher frequency of consciousness declination (p = 0.029), and a higher modified Rankin scale (mRS) score during hospitalization. Low fT3 levels were also associated with abnormal MRI findings, a decline in consciousness, and the mRS score on admission. In addition, fT3 seemed to gradually return to normal levels upon improvement of the mRS score (r = –0.649, p = 0.002). Conclusions: Low T3 syndrome often copresents in anti-NMDAR encephalitis and indicates a longer hospitalization, abnormal MRI findings, consciousness declination, and a higher clinical severity. However, fT3 levels do not seem to influence the prognosis of anti-NMDAR encephalitis.

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Section: Discussionsupporting

confidence: 49%

Thyroid Function and Autoimmune Indications in Patients with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

Ma¹,

Yin²,

Zeng³

et al. 2018

Neuroimmunomodulation

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“…THs regulate systemic glucose metabolism and also are involved in the regulation of the brain glucose metabolism (Jahagirdar & McNay, ). The part of the present study concerning brain glucose metabolism showed a decreased amount of two important glycolytic enzymes, Hexokinase and phosphofructokinase, and lower concentrations of one of the products of glycolysis, lactate, in the 90 ‐day old PFC and hippocampus of the BPA–exposed rats.…”

Section: Discussionmentioning

confidence: 99%

“…The regional deiodinases are critical determinants of the local T 3 pool and therefore modulate nuclear T 3 concentration and TR saturation. In rat brain, the local DIO2 activity is responsible for over 80% of the local T 3 production (Crantz, Silva, & Larsen, 1982 THs regulate systemic glucose metabolism and also are involved in the regulation of the brain glucose metabolism (Jahagirdar & McNay, 2012). The part of the present study concerning brain glucose metabolism showed a decreased amount of two important glycolytic enzymes, Hexokinase and phosphofructokinase, and lower concentrations of one of the products of glycolysis, lactate, in the 90 -day old PFC and hippocampus of the BPA-exposed rats.…”

Section: Discussionmentioning

confidence: 99%

The effects of perinatal bisphenol A exposure on thyroid hormone homeostasis and glucose metabolism in the prefrontal cortex and hippocampus of rats

et al. 2019

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Introduction Bisphenol A (BPA) is an endocrine disruptor widely used to manufacture consumer goods. Although the thyroid hormone (TH) disrupting potential of BPA has been thought to be responsible for the neuropsychiatric deficits in the animals that experienced perinatal BPA exposure, the TH availability change at the level of specific brain structures has not been subject to systematic investigation. Methods In the present study the impacts of perinatal BPA exposure (0.1 mg/L in drinking water) spanning gestation and lactation on TH homeostasis in the prefrontal cortex (PFC) and hippocampus were assessed in male Sprague–Dawley rats at postnatal day 21 (PND21) and PND90. As TH regulates brain glucose metabolism at multiple levels，the effects of BPA treatment on glucose metabolism in the brain tissues were also assessed in adult rats. Results The results showed heterogeneous changes in TH concentration induced by BPA between serum and brain tissues, additionally, in the BPA–treated pups, up–regulated expression of the TH transporter monocarboxylate 8 mRNA at PND21 and increased type 3 iodothyronine deiodinase mRNA expressions at PND21 and PND90 were observed. Meanwhile, decreased glucose metabolism was seen in the PFC and hippocampus, while deficits in locomotor activity, spatial memory and social behaviors occurred in BPA‐treated groups. Conclusion These data support the concept that the developing brain possesses potent mechanisms to compensate for a small reduction in serum TH, such as serum hypothyrodism induced by BPA exposure, however, the long‐term negative effect of BPA treatment on TH homeostasis and glucose metabolism may be attributable to neuropsychiatric deficits after mature.

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“…Thus, the reduced spontaneous activity of RH animals is unlikely to be due to any physical impairment but is rather due to altered internal drive. One possible explanation for altered energy expenditure might have been an alteration in thyroid function, and it has been recently suggested that thyroid hormone may regulate both insulin signaling and hippocampal function (21). Although the RH animals became larger, hence requiring additional energy expenditure for a given amount of motor activity, the reduction in activity appears to be greater than could be explained by this variable alone: at 12 mo, RH animals were 69.5% heavier on average than control animals, but control animals' activity was 132% higher than that of the RH animals.…”

Section: Discussionmentioning

confidence: 99%

Long-term, intermittent, insulin-induced hypoglycemia produces marked obesity without hyperphagia or insulin resistance: A model for weight gain with intensive insulin therapy

McNay¹,

Teske

Kotz

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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A major side effect of insulin treatment of diabetes is weight gain, which limits patient compliance and may pose additional health risks. Although the mechanisms responsible for this weight gain are poorly understood, it has been suggested that there may be a link to the incidence of recurrent episodes of hypoglycemia. Here we present a rodent model of marked weight gain associated with weekly insulin-induced hypoglycemic episodes in the absence of diabetes. Insulin treatment caused a significant increase in both body weight and fat mass, accompanied by reduced motor activity, lowered thermogenesis in response to a cold challenge, and reduced brown fat uncoupling protein mRNA. However, there was no effect of insulin treatment on total food intake nor on hypothalamic neuropeptide Y or proopiomelanocortin mRNA expression, and insulin-treated animals did not become insulin-resistant. Our results suggest that repeated iatrogenic hypoglycemia leads to weight gain, and that such weight gain is associated with a multifaceted deficit in metabolic regulation rather than to a chronic increase in caloric intake.

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Thyroid hormone’s role in regulating brain glucose metabolism and potentially modulating hippocampal cognitive processes

Cited by 28 publications

References 181 publications

Thyroid Function and Autoimmune Indications in Patients with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

Thyroid Function and Autoimmune Indications in Patients with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

The effects of perinatal bisphenol A exposure on thyroid hormone homeostasis and glucose metabolism in the prefrontal cortex and hippocampus of rats

Long-term, intermittent, insulin-induced hypoglycemia produces marked obesity without hyperphagia or insulin resistance: A model for weight gain with intensive insulin therapy

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