Plasma insulin and C-peptide in relation to glucose intolerance in middle-aged men
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Abstract. The relation between glucose homeostasis and insulin secretion (immunoreactive insulin and C-peptide) was studied in middle-aged males matched for age and body weight. Subjects with mild type II diabetes mellitus were compared to normals and to individuals with impaired glucose tolerance (IGT). In addition, the diabetics were subdivided according to duration, some of the subjects having recently deteriorated from IGT status. In the IGT individuals, there were no indications of a reduction in basal or glucose-induced insulin output. On the contrary, data indicate somewhat higher than normal secretion. Within the type II diabetics, those of short duration were largely similar to normals, whereas diabetes of longer duration was associated with some diminution in indices of B cell secretion. The data support the notion that a deficient insulin output is not a primary pathophysiological event in the development of type II diabetes.Keywords:
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C-peptide
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Pathophysiology
Abstract Humans living at a higher altitude are less prone to suffer from impaired glucose homeostasis and type 2 diabetes mellitus (T2DM), which might at least partly be explained by lower oxygen availability at higher altitudes. The present systematic review aimed to provide an overview of the current literature on the effects of hypoxia exposure on glucose homeostasis in metabolically compromised humans. Several databases were searched up to August 10 th , 2020. The search strategy identified 368 unique records. Following assessment for eligibility based on the selection criteria, 16 studies were included in this review. Six studies (2 controlled studies; 4 uncontrolled studies) demonstrated beneficial effects of hypoxia exposure on glucose homeostasis, while 10 studies (8 controlled studies; 2 uncontrolled studies) reported no improvement in glucose homeostasis following hypoxia exposure. Notably, passive hypoxia exposure seemed to improve glucose homeostasis, whereas hypoxic exercise training (2–8 weeks) appeared to have no additional/synergistic effects on glucose homeostasis compared to normoxia exposure. Due to the heterogeneity in study populations and intervention duration (acute studies / 2–8 wks training), it is difficult to indicate which factors may explain conflicting study outcomes. Moreover, these results should be interpreted with some caution, as several studies did not include a control group. Taken together, hypoxia exposure under resting and exercise conditions might provide a novel therapeutic strategy to improve glucose homeostasis in metabolically compromised individuals, but more randomized controlled trials are warranted before strong conclusions on the effects of hypoxia exposure on glucose homeostasis can be drawn.
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Glucose homeostasis is very tightly controlled to allow constant availability of fuel to cells in fed, fasted and exercise states. The control of glucose requires a co-ordinated effort over several organs. For example, maintenance of glucose homeostasis relies on neuronal and hormonal control of the liver to switch between glucose uptake and glucose release. Major hormonal control of the liver comes from the secretion of glucagon and insulin from the pancreas. However it is now known that other hormones in the entero-insular axis, which includes the pancreas and the gastrointestinal (GI), also contribute to the regulation of glucose homeostasis. The importance of glycaemic control becomes apparent when glucose homeostasis is disrupted leading to metabolic diseases such as diabetes mellitus. Currently, the major aim for diabetic patients is to maintain adequate control of glycaemia to lower the risk of complications associated with glucose fluctuations including kidney disease, cardiovascular complications and blindness. New understanding of the roles of other hormones has led to a multi-hormonal view of glucose homeostasis and as such, increased the potential for therapeutic targets to be developed. Three peptides were investigated in this thesis for their potential as glucoregulatory hormones. Preptin is a 34 amino acid peptide isolated from the granules of ??TC6-F7 cells, an islet ??-cell line and corresponds to the E domain of proIGF-2. Although isolated from a ??-cell line, preliminary studies indicated preptin-like immunoreactivity (PLIM) is confined to the ??-cell in the pancreas and as yet unidentified cells in the mucosa of the stomach of rats. In addition, preptin has been shown to be co-secreted with insulin in ??TC6-F7 cells and to increase glucose-stimulated insulin secretion (GSIS) in the rat pancreas. This thesis investigated the location of preptin in the stomach. However PLIM was not able to be confirmed due to lack of a suitable antibody. Furthermore, two alternative methods, MALDI-TOF and LC-MS/MS did not detect preptin in the rat pancreas. Therefore the presence of preptin in rat islets is inconclusive. Preptin effects on liver function were also investigated in an isolated perfused rat liver model. While preptin decreased glucose output, its effects were insubstantial and inconsistent compared to the well-characterised glucoregulatory hormone, insulin. However, the presence of other PLIM products in disease indicate that proIGF-2 may have a physiological role and further investigation is warranted to elucidate proIGF-2 products in the pathology of metabolic diseases. Two peptides were also investigated as glucoregulatory peptides. GRPP was purified from the porcine pancreas and studies using MALDI-TOF also suggested its presence in rat and mouse islets. Glicentin-related pancreatic polypeptide-like peptide (GRPP-LP) was discovered in rat islets using MALDI-TOF and LC-MS/MS techniques. This thesis studied the effect of rat GRPP and rat GRPP-LP in the isolated perfused rat liver, however no…
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Abstract The brain, particularly the ventromedial hypothalamic nucleus (VMH), has been long known for its involvement in glucose sensing and whole-body glucose homeostasis. However, it is still not fully understood how the brain detects and responds to the changes in the circulating glucose levels, as well as brain-body coordinated control of glucose homeostasis. In this review, we address the growing evidence implicating the brain in glucose homeostasis, especially in the contexts of hypoglycemia and diabetes. In addition to neurons, we emphasize the potential roles played by non-neuronal cells, as well as extracellular matrix in the hypothalamus in whole-body glucose homeostasis. Further, we review the ionic mechanisms by which glucose-sensing neurons sense fluctuations of ambient glucose levels. We also introduce the significant implications of heterogeneous neurons in the VMH upon glucose sensing and whole-body glucose homeostasis, in which sex difference is also addressed. Meanwhile, research gaps have also been identified, which necessities further mechanistic studies in future.
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Glucose homeostasis is maintained through interplay between central and peripheral control mechanisms which are aimed at storing excess glucose following meals and mobilizing these same stores during periods of fasting. The nucleus of the solitary tract (NST) in the dorsal medulla has long been associated with the central detection of glucose availability and the control of glucose homeostasis. Recent evidence has emerged which supports the involvement of astrocytes in glucose homeostasis. The aim of the present study was to investigate whether NST-astrocytes respond to physiologically relevant decreases in glucose availability, in vitro, as well as to the presence of the glucoprivic compound 2-deoxy-D-Glucose. This report demonstrates that some NST-astrocytes are capable of responding to low glucose or glucoprivation by increasing cytoplasmic calcium; a change that reverses with restoration of normal glucose availability. While some NST-neurons also demonstrate an increase in calcium signaling during low glucose availability, this effect is smaller and somewhat delayed compared to those observed in adjacent astrocytes. TTX did not abolish these hypoglycemia mediated responses of astrocytes, suggesting that NST-astrocytes may be directly sensing low glucose levels as opposed to responding to neuronal detection of hypoglycemia. Thus, chemodetection of low glucose by NST-astrocytes may play an important role in the autonomic regulation of glucose homeostasis.
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Using a composite model of the glucose homeostasis system, consisting of seven interconnected submodels, we enumerate the possible behaviours of the model in response to variation of liver insulin sensitivity and dietary glucose variability. The model can reproduce published experimental manipulations of the glucose homeostasis system and clearly illustrates several important properties of glucose homeostasis-boundedness in model parameters of the region of efficient homeostasis, existence of an insulin sensitivity that allows effective homeostatic control and the importance of transient and oscillatory behaviour in characterizing homeostatic failure. Bifurcation analysis shows that the appearance of a stable limit cycle can be identified.
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