Serum leptin levels are not influenced by physical training in type 2 diabetes mellitus patients

Ligtenberg, P. C.; Hoekstra, J. B. L.; Frölich, Marijke; Meinders, A. E.; Erkelens, D. W.

doi:10.1046/j.1463-1326.1999.00004.x

Cited by 3 publications

(2 citation statements)

References 28 publications

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“…axis functions (endocrines, circadian rhythms, etc.). It is quite possible that, similarly in similar human cases, an equivalent defective receptor mutation, also localized in chromosome 7q, translates into faulty leptin receptor causing congenital obesity [54][55][56][57][58][59][60][61][62][63][64][65][66]88,244,246,[261][262][263][264] that can influence insulin activity. 38,[54][55][56][57][58][59][60][61][62][63][64][65][66]263,264 In these human cases, demyelination defects have yet to be found and studied.…”

Section: The Myelin and Possible Causes Of The Damagesmentioning

confidence: 99%

“…Interestingly, the Zucker obese rats bore myelin anomalies resembling the ones found in toxicantinduced diabetes in animals [43][44][45][46][47][48][49][50][51][52] and probably also thosenot studied by fine structurefound in unusual human cases of diabetes where leptin receptor was similarly incompetent. [53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69] Therefore, the discussion of our demyelination data includes diabetes type 2 considerations along with leptin-linked endocrine interactions.…”

Section: Introductionmentioning

confidence: 99%

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The leptin receptor mutation of the obese Zucker rat causes sciatic nerve demyelination with a centripetal pattern defect

Gilloteaux

Subramanian

Solomon

et al. 2018

Ultrastructural Pathology

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Young male Zucker rats with a leptin receptor mutation are obese, have a non-insulin-dependent diabetes mellitus (NIDDM), and other endocrinopathies. Tibial branches of the sciatic nerve reveal a progressive demyelination that progresses out of the Schwann cells (SCs) where electron-contrast deposits are accumulated while the minor lines or intermembranous SC contacts display exaggerated spacings. Cajal bands contain diversely contrasted vesicles adjacent to the abaxonal myelin layer with blemishes; they appear dispatched centripetally out of many narrow electron densities, regularly spaced around the myelin annulus. These anomalies widen and yield into sectors across the stacked myelin layers. Throughout the worse degradations, the adaxonal membrane remains along the axonal neuroplasm. This peripheral neuropathy with irresponsive leptin cannot modulate hypothalamic-pituitaryadrenal axis and SC neurosteroids, thus exacerbates NIDDM condition. Additionally, the ultrastructure of the progressive myelin alterations may have unraveled a peculiar, centripetal mode of trafficking maintenance of the peripheral nervous system myelin, while some adhesive glycoproteins remain between myelin layers, somewhat hindering the axon mutilation. Heading title: Peripheral neuropathy and myelin ARTICLE HISTORY

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Section: The Myelin and Possible Causes Of The Damagesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The leptin receptor mutation of the obese Zucker rat causes sciatic nerve demyelination with a centripetal pattern defect

Gilloteaux

Subramanian

Solomon

et al. 2018

Ultrastructural Pathology

View full text Add to dashboard Cite

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Physical activity and adipokine levels in individuals with type 2 diabetes: A literature review and practical applications

Zarekookandeh

Haghighi

Daraei

et al. 2021

Rev Endocr Metab Disord

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The effects of physical activity on adipokines in individuals with overweight/obesity across the lifespan: A narrative review

et al. 2020

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Summary This narrative review summarizes current knowledge on the effects of physical activity (PA) on adipokine levels in individuals with overweight and obesity. Approximately 90 investigations including randomized control, cross‐sectional and longitudinal studies that reported on the effects of a single session of PA (acute) or long‐term PA (chronic) on adipokine levels in individuals with overweight/obesity were reviewed. The findings support the notion that there is consensus on the benefits of chronic exercise training—regardless of the mode (resistance vs. aerobic), intensity and cohort (healthy vs. diabetes)—on adipokine levels (such as tumour necrosis factor‐alpha, interleukin‐6, adiponectin, visfatin, omentin‐1 and leptin). However, several confounding factors (frequency, intensity, time and type of exercise) can alter the magnitude of the effects of an acute exercise session. Available evidence suggests that PA, as a part of routine lifestyle behaviour, improves obesity complications by modulating adipokine levels. However, additional research is needed to help identify the most effective interventions to elicit the most beneficial changes in adipokine levels in individuals with overweight/obesity.

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Serum leptin levels are not influenced by physical training in type 2 diabetes mellitus patients

Abstract: No effect of physical training on leptin levels was detectable in elderly, obese type 2 diabetes mellitus patients.

Cited by 3 publications

References 28 publications

The leptin receptor mutation of the obese Zucker rat causes sciatic nerve demyelination with a centripetal pattern defect

The leptin receptor mutation of the obese Zucker rat causes sciatic nerve demyelination with a centripetal pattern defect

Physical activity and adipokine levels in individuals with type 2 diabetes: A literature review and practical applications

The effects of physical activity on adipokines in individuals with overweight/obesity across the lifespan: A narrative review

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