Effects of streptozotocin-induced diabetes on taste buds in rat vallate papillae

Pai, Man Hui; Ko, Tsui-Ling; Chou, Hsiu Chu

doi:10.1016/j.acthis.2006.10.006

Cited by 16 publications

(14 citation statements)

References 37 publications

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“…Taste buds of diabetic rats exhibit enhanced expression of ␣-gustducin protein and reduced expression of the sweet taste receptor TAS1R3, which may partially explain the sweet taste disorders observed in the diabetic context (96,97). Although morphometry studies have shown that diabetic rats present no significant difference in papillae size compared with control animals, the innervation of these taste cells is significantly reduced (71). Therefore, the attenuation of sweetness perception may trigger sweet-seeking behaviors in some individuals, potentially increasing the risk of overconsumption of high-energy foods (e.g., rich in glucose) and eventually contributing to the development of obesity (49).…”

Section: Glucosensing In the Oral Cavitymentioning

confidence: 79%

Glucosensing in the gastrointestinal tract: Impact on glucose metabolism

Fournel

Marlin

Abot

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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The gastrointestinal tract is an important interface of exchange between ingested food and the body. Glucose is one of the major dietary sources of energy. All along the gastrointestinal tube, e.g., the oral cavity, small intestine, pancreas, and portal vein, specialized cells referred to as glucosensors detect variations in glucose levels. In response to this glucose detection, these cells send hormonal and neuronal messages to tissues involved in glucose metabolism to regulate glycemia. The gastrointestinal tract continuously communicates with the brain, especially with the hypothalamus, via the gut-brain axis. It is now well established that the cross talk between the gut and the brain is of crucial importance in the control of glucose homeostasis. In addition to receiving glucosensing information from the gut, the hypothalamus may also directly sense glucose. Indeed, the hypothalamus contains glucose-sensitive cells that regulate glucose homeostasis by sending signals to peripheral tissues via the autonomous nervous system. This review summarizes the mechanisms by which glucosensors along the gastrointestinal tract detect glucose, as well as the results of such detection in the whole body, including the hypothalamus. We also highlight how disturbances in the glucosensing process may lead to metabolic disorders such as type 2 diabetes. A better understanding of the pathways regulating glucose homeostasis will further facilitate the development of novel therapeutic strategies for the treatment of metabolic diseases.glucosensing; glucose homeostasis; diabetes GLUCOSE REPRESENTS ONE of the major sources of energy circulating throughout the body. The tight and continuous control of glycemia in the face of fluctuations in glucose absorption, storage, and production is crucial for all living organisms. Not surprisingly, the gastrointestinal tract constitutes the first anatomic site for the detection of nutrients, including glucose. Glucose detection involves specialized cells referred to as glucosensors (21,44,64). These cells, which are present in the oral cavity as well as the small intestine, pancreas, and portal vein, express various glucose transporters and G proteincoupled receptors (GPCRs) implicated in the physiological response to glucosensing (21,44,64). Glucosensing by these cells evokes complex neural and endocrine responses that control glucose metabolism. Moreover, glucose detection in the gastrointestinal tract also transmits afferent nervous impulses to the brain, which, in turn, controls peripheral glucose utilization. Indeed, the brain, specifically the hypothalamus, is a key player in the regulation of glucosensing mechanisms. In addition to receiving information via the gut-brain axis, the hypothalamus also contains glucosensitive cells able to detect glucose (91). Upon the integration of these messages, the hypothalamus sends specific signals to the tissues involved in glucose metabolism via the autonomous nervous system (ANS).Metabolic disorders such as type 2 diabetes (T2D) are considered as ...

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Section: Glucosensing In the Oral Cavitymentioning

confidence: 79%

Glucosensing in the gastrointestinal tract: Impact on glucose metabolism

Fournel

Marlin

Abot

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Fine neurofilament and PGP 9.5 immunopositive intragemmal fibres were present within many taste buds in vallate and foliate papillae (Fig 4b). Oval PGP 9.5 immunoreactive cells were observed within taste buds (Fig 4b), as occurs in rats [20], but contrasting with human subjects where PGP 9.5 immunopositivity was strictly localised to nerve fibres [17]. Neurofilament immunopositivity within taste buds was strictly localised in nerve fibres (Fig 4c).…”

Section: General Structure Of the Equine Subgemmal Plexus And Gustatomentioning

confidence: 81%

Neuronal chromatolysis in the subgemmal plexus of gustatory papillae in horses with grass sickness

McGorum

Pirie

Shaw

et al. 2015

Equine Veterinary Journal

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“…A neuronal glucose detection begins inside the mouth, in the gustative papilleae of the tongue innervated by the vagus nerve and the lingual enteric nervous system (LENS) and where reside also a prokaryotic community, the oral microbiota. The neuronal glucose detection is critical for the metabolism control staining, western blot of BCL2, BAX and activated caspase 3 and 9 and immunostaining of PGP9.5, a neuronal marker in the taste buds of diabetic rats [39,40]. Thus, these alterations of the tongue detection described by the decrease of the sensor cells or neuronal innervation inside the taste buds or an alteration of some intracellular signaling can induce an alteration of the food intake and food preferences leading to aggravate metabolic diseases.…”

Section: Vagus Nerve Enteric Nervous System and Their Alterations Dumentioning

confidence: 99%

The gut microbiota to the brain axis in the metabolic control

Grasset

Burcelin

2019

Rev Endocr Metab Disord

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The regulation of glycemia is under a tight neuronal detection of glucose levels performed by the gut-brain axis and an efficient efferent neuronal message sent to the peripheral organs, as the pancreas to induce insulin and inhibit glucagon secretions. The neuronal detection of glucose levels is performed by the autonomic nervous system including the enteric nervous system and the vagus nerve innervating the gastro-intestinal tractus, from the mouth to the anus. A dysregulation of this detection leads to the one of the most important current health issue around the world i.e. diabetes mellitus. Furthemore, the consequences of diabetes mellitus on neuronal homeostasis and activities participate to the aggravation of the disease establishing a viscious circle. Prokaryotic cells as bacteria, reside in our gut. The strong relationship between prokaryotic cells and our eukaryotic cells has been established long ago, and prokaryotic and eukaryotic cells in our body have evolved synbiotically. For the last decades, studies demonstrated the critical role of the gut microbiota on the metabolic control and how its shift can induce diseases such as diabetes. Despite an important increase of knowledge, few is known about 1) how the gut microbiota influences the neuronal detection of glucose and 2) how the diabetes mellitus-induced gut microbiota shift observed participates to the alterations of autonomic nervous system and the gut-brain axis activity.

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Effects of streptozotocin-induced diabetes on taste buds in rat vallate papillae

Cited by 16 publications

References 37 publications

Glucosensing in the gastrointestinal tract: Impact on glucose metabolism

Glucosensing in the gastrointestinal tract: Impact on glucose metabolism

Neuronal chromatolysis in the subgemmal plexus of gustatory papillae in horses with grass sickness

The gut microbiota to the brain axis in the metabolic control

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