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In mice, the glucose administration was done both orally and intraperitoneally to determine the oral glucose tolerance test and the IP glucose tolerance test. Using the AlphaTRAK blood glucose monitoring device, glucose levels in blood were determined by performing tail bleeds at 0, 15, 30, 60, 90, and 120 min. The blood glucose level was elevated to the maximum level at 15 min after glucose administration, according to the study. In 4-copy mice, the blood glucose levels were also significantly lower than those in 2-copy mice than in 2-copy mice. OGTT had a significantly reduced rate of maximal blood glucose when compared to IPGTT. The presence of Npr1 in the regulation of glucose homeostasis and mutant animals' glucose levels are shown by the present study.
Source link: https://europepmc.org/article/MED/35556934
A key regulator of hepatic and systemic insulin sensitivity is the hepatic transcription factor for the box O1's. Both in genetic and dietary mouse models of metabolic disease, our group and others' research showed that genetic inhibition of FOXO1 enhances insulin sensitivity. Hepatic FOXO1-controlled One candidate hepatokine controlled by hepatic FOXO1 is the fibroblast growth factor 21. We performed acute loss-of-function experiments to determine the role of hepatocyte-derived FGF21 in glucose homeostasis and insulin resistance in both rats and mice lacking hepatic insulin signaling in this paper.
Source link: https://europepmc.org/article/MED/35303074
The aim of the current research was to determine whether paternal eNOS deficiency could result in the same phenotype as seen with maternal eNOS deficiency. Male eNOS were bred with female wild-type mice or wild-type male mice, killing mice or wild-type male mice. Compared to offspring from wild-type parents, the phenotype of heterozygous male eNOS knockout mice was similar to those of wild-type offspring. Global sperm DNA methylation decreased, and sperm microRNA pattern changed dramatically. According to our report, paternal genetic anomalies such as eNOS deficiency may alter the sperm's epigenome, without the paternal genetic defect itself. After glucose load, the fathers' wild-type male offspring of +/-eNOS fathers developed more fasting insulin and elevated insulin levels in later life.
Source link: https://europepmc.org/article/MED/35488925
Mice were immediately intracerebroventricular injection of 26RFa, insulin, or the 26RFa receptor antagonist 25e, as well as IPGTTs, insulin tolerance testing, acute glucose-stimulated insulin secretion testing, and pyruvate tolerance testing were performed. neurons expressing 26Rfa are mainly localized in the lateral hypothalamic zone, and insulin co-express the gene encoding the insulin receptor and the expression of 26Rfa in these neurons, according to RNAscope experiments. Additionally, our results show that hypothalamic 26RFa neurons are not involved in the central inhibitory effect of insulin on hepatic glucose manufacture, but that the hormone's central effects on peripheral production are not involved. We have developed a novel device in the hypothalamic regulation of glucose homeostasis, the 26RFa/GPR103 system, and we have evidence that this neuronal peptidergic system is a key relay for insulin-mediated regulation of glucose metabolism.
Source link: https://europepmc.org/article/MED/35476025
AMPK and mTORC1 are both involved in controlling cell metabolism by folliculin interacting protein 1. However, it is unclear if and how FNIP1 regulates adipocyte browning. FNIP1 binds to and promotes SERCA, a key Ca2+ pump that is responsible for cytosolic Ca2+ removal by mechanistically. FNIP1's loss resulted in elevated intracellular Ca2+ signals and the subsequent activation of a Ca2+-dependent thermogenic program in adipocytes. These findings point to a pivotal role for FNIP1 as a negative regulator of beige adipocyte thermogenesis and unraveling an intriguing functional link between intracellular Ca2+ dynamics and adipocyte browning.
Source link: https://europepmc.org/article/MED/35412553
Here we show that elevated adipocyte lipolysis can be prevented by selective activation of adipocyte G q signaling in vitro and in vivo by using a multi-genetic/pharmacologic approach. Activation of this pathway by a G q-coupled designer receptor or an agonist acting on an endogenous adipocyte G q -coupled receptor has significantly increased glucose and lipid homeostasis in obese mice or mice with adipocyte insulin receptor deficiency.
Source link: https://europepmc.org/article/MED/35351896
Medium-chain triglycerides, triglyceride derivatives of medium-chain fatty acids, are widely used to satisfy athletes, the elderly, and people with stumbling growth because MCFAs are converted into energy for immediate use by the organs and do not accumulate as fat. Methods MCTs or MCFAs were administered to male GPR84-deficient mice with a C57BL/6J background and mouse enteroendocrine cell line STC-1, along with mouse enteroendocrine cell line STC-1, and mouse enteroendocrine cell line STC-1, evaluating glucose homeostasis and gut hormone GLP-1 secretion. Each MCT intake differed in terms of lard intake and increased metabolic levels. In addition, C10:0 stimulation in STC-1 enhanced glucose tolerance by GPR84-mediated GLP-1 secretion, improved glucose tolerance in mice, and showed resistance to high-fat diet-induced obesity in mice. Conclusions Dietary MCT intake effectively can help reduce obesity and insulin resistance by GLP-1 mision.
Source link: https://europepmc.org/article/MED/35399667
We did a 12-week review in a VPAC1R null model to better identify the effects of VPAC1R on body phenotype, energy/glucose homeostasis, and metabolism. Our findings show that VPAC1-/- mice underwent significant metabolic changes during the dark cycle, including greater numbers of feeding bouts, lower Total Energy Expenditure, VO2, and VCO2; as well as during the light cycle with lower Total Energy Expenditure, VO2, and VCO2 ; among others. In addition, VPAC1-/- mice had significantly higher GLP-1 and PYY during fasting, as well as elevated GLP-1, glucagon leptin, and PYY during postprandial conditions.
Source link: https://europepmc.org/article/MED/35336804
Scope Obesity is becoming a significant public health issue due to a high intake of saturated fats. Dendrobium officinale, a medicine food homology plant, has multiple health benefits and is capable of a variety of health-promoting activities. Methods and findings By gavage for 11 weeks, high-fat diet -fed mice are administered D. officinale dietary fiber daily by gavage for 11 weeks. After DODF therapy was successful in obese mice by increasing insulin pathway and hepatic glycogen synthesis, improved glucose homeostasis was found in obese mice. DODF restructures the intestinal microbiota in obese mice by reducing the relative abundance of Bilophila and increasing the relative abundances of Akkermansia, Bifidobacterium, and Muribaculum. FMT has a part of these health-related diseases, which puts the gut microbiota as a target for DODF's protective effects on obesity-related disorders. Conclusions The results show that DODF can be used as a novel prebiotic to maintain intestinal microbial balance and improve metabolic stability, reducing hunger and related metabolic syndrome.
Source link: https://europepmc.org/article/MED/35225418
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