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Pinch1/2 proteins are significantly elevated in white adipose tissue in mice thanks to a high-fat diet. In addition, Pinch1 expression in WAT in leptin-deficient ob/ob type 2 diabetic mice and obese humans is largely restricted. While mice lacking Pinch1 in adipocytes or global Pinch2 have no apparent phenotypes, they do not have any notable phenotypes, such as brown adipose tissue mass, but not brown adipocytes and Pinch2 tissue mass in HFD-fed, but not normal chow diet-fed mice. While Pinch loss reduces adipocyte size and alters adipocyte size distribution, it nonetheless accelerates cell apoptosis, particularly in epididymal WAT and to a lesser extent in subcutaneous WAT. In vivo, genetic inadipocyte expression of Caspase-8 in adipocytes has effectively ended the ameliorating effects of Pinch deficiency on obesity, glucose intolerance, and fatty liver in mice.
Source link: https://doi.org/10.2337/db21-0392
Since TRF is on the rise, and feeding may be interrupted in those that are pregnant, it is vital to know the resultant offspring's long-term effects. We tested the effects of gestational exposure to early TRF on both male and female offspring using a mouse model. In both males and females from weaning to adulthood, both males and females, the offspring body composition remained similar, with minor changes in food intake in eTRF females and improved glucose tolerance in males. Male eTRF offspring were more sensitive to insulin after ten weeks of high fat, high sucrose diet feeding, but insulin resistance was exacerbated by impaired insulin secretion. After persistent high fat, high sucrose diet feeding in male offspring, gestational eTRF has gender-specific deleterious effects on glucose homeostasis.
Source link: https://doi.org/10.1101/2022.04.27.489576
According to the PGK's promoter, we have seen a decrease in insulin secretion and glucose intolerance in young mice overexpressing human IGFBP-3 or its mutant Gly76/Gly80/Gly81-IGFBP-3. Here, we looked at studies comparing glucose and lipid homeostasis in PGK and PGKmut3 mice with age in PGKBP3 and PGKmut3 mice to wild-type mice. IGFBP-3 in all mouse genotypes was similar to previous mouse genotypes and decreased with age in parallel with total IGF-1. In PGKmutBP3 mice, visceral fat and BAT masses increased, but not in PGKBP3 mice. Both PGKmutBP3 and PGKmutBP3 mice had elevated glycerol in the blood, but only PGKBP3 mice had elevated free fatty acids and only PGKmutBP3 mice had elevated triglycerides, and only PGKmutBP3 mice had elevated triglycerides. So, overexpression of human IGFBP-3 or its mutant forms of IGF binding ability leads to glucose intolerance in young mice, but there are also variations on insulin secretion, insulin sensitivity, and lipid homeostasis in elderly mice.
Source link: https://doi.org/10.1210/en.2014-1271
Male and female GHA and wild-type mice in a C57BL/6 background were placed on HF and low-fat diets for 11 weeks, starting at 10 weeks of age, to see how GHA mice respond to additional metabolic strain from HF feeding. Both mice on a HF diet gained weight, although GHA gained more weight than WT mice, with males rising more than females on a HF diet. The majority of this weight gain was due to an increase in fat mass in WT mice's white adipose tissue perigonadal depots, while GHA mice gained in both the sc and perigonadal white adipose tissue regions. Notably, GHA mice were somewhat shielded from adverse glucose metabolism changes on a HF diet because they had only modest rises in serum glucose levels, remained glucose tolerant, and did not experience hyperinsulinemia.
Source link: https://doi.org/10.1210/en.2014-1617
After oral glucose loading, GIPR//= mice have elevated blood glucose levels and delayed initial insulin response. After oral glucose load in vivo, early insulin secretion mediated by GIP determines glucose tolerance, and because GIP plays a key role in the compensatory increase of insulin secretion produced by a high insulin demand, a defect in this entero-insular axis could lead to diabetes pathogenesis.
Source link: https://doi.org/10.1073/pnas.96.26.14843
These other synaptotagmins may act as Ca 2+ transducers governing other Ca 2+-dependent membrane reactions, such as insulin secretion in pancreatic -cells, by analogy to synaptotagmin-1, -2, and -9 in neurotransmission. Synaptotagmin-7 is one of the most abundant among these other synaptotagmins, and it is abundant in pancreatic -cells. To see if synaptotagmin-7 regulates Ca 2+ -dependent insulin secretion, we tested synaptotagmin-7 null mutant mice for glucose tolerance and insulin release. Synaptotagmin-7 is required for systemic glucose tolerance maintenance and glucose-stimulated insulin secretion, according to this page. Our results show that synaptotagmin-7 is a positive regulator of insulin secretion and may act as a calcium sensor monitoring insulin secretion in pancreatic cells, which can be taken together.
Source link: https://doi.org/10.1073/pnas.0711700105
ABSTRACT Background Although diet selenium deficiency or excess in mice causes type 2 diabetes-like signs in mice, the suboptimal body Se status often causes no signs, but may contribute to an age-related decline in overall wellbeing. Objects We investigated to find out what dietary Se dietary Se requirement for immunity against type 2 diabetes-like symptoms in mice. Methods For 4 mo until they were middle-aged, mature male C57BL/6J mice were fed a Se-deficient torula yeast AIN-93M diet supplemented with Na2SeO4 in graded concentrations of 0. 01, 0. 04, 0. 10, 0. 10, and 0. 13 mg Se/kg for 4 mo. Middle-aged mice's serum insulin and leptin concentrations increased relative to control's control. Conclusions Mice fed diets that contain 0. 10 mg Se/kg demonstrate impaired glucose tolerance and insulin sensitivity, raising the risk of type 2 diabetes in women with suboptimal Se status at levels 23% of dietary requirements.
Source link: https://doi.org/10.1093/jn/nxab053
In mice, knockout of RIII, the main PKA regulatory subunit in adipose tissue, or knockout of the catalytic subunit C led to a lean phenotype that resists diet-induced obesity and related metabolic difficulties. RIIKO mice weighed less than wild-type littermates after two weeks of high-fat diet exposure. Decreased intake of a high-fat diet contributed to the attenuated weight gain in RIIKO mice. In addition, RIII's deficiency caused differential monitoring of PKA in primary metabolic organs: cAMP-stimulated PKA activity was reduced in liver and increased in gonadal adipose tissue.
Source link: https://doi.org/10.1210/en.2014-1122
T cells are thought to be responsible for age-related glucose intolerance, as reported in the previous study. In otherwise healthy animals, the aim of this research was to examine the possibility that early life thymectomy at 3wks of age causes T cell death and subsequent glucose homeostasis. Male C57BL6 mice underwent thymectomy or sham surgery at 3wks of age. Following euthanasia at 9 mo of age, splenic T cell phenotype was determined by flow cytometry. During the GTT, 6 million old thymex mice had a larger area under the curve than controls. Thymex mice had a reduced splenic CD4:CD8 ratio relative to controls and a trend toward a memory CD8+ T cell phenotype, which is all consistent with age. This finding shows that early life thymectomy may raise T cell aging, resulting in glucose tolerance impairments in otherwise healthy and middle-aged mice.
Source link: https://doi.org/10.1093/geroni/igab046.2542
In mice, we therefore investigated the role of SR-BI in mice's high fat diet-induced obesity. Methods and Results: Male SR-BI knockout and wild-type mice were fed a diet containing 45% energy as fat for 12 weeks. Compared to WT mice with elevated fasting levels of free cholesterol, cholesterol esters, triglycerides, and glucose, SR-BI KO mice had an elevated metabolic plasma profile. For WT, the SR-BI KO weighed 4. 5 g versus 4. 2 g. SR-BI KO mice' relative body mass increase over time was noticeably higher in SR-BI KO mice as compared to WT controls. The SR-BI deficiency is thus uncoupling obesity in mice, which also leads to obesity due to glucose intolerance. Conclusions: Our experiments for the first time show that a proper SR-BI system prevents mouse obesity formation.
Source link: https://doi.org/10.1161/circ.132.suppl_3.19498
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