Identification of herbal drug extracts that promote growth of in high-fat diet fed mice.

Unlabelled: Disruption of the gut microbiota causes metabolic dysfunction, and intervention in the gut microbiota has the potential to improve host glucose metabolism. is an intestinal bacterium involved in anti-obesity and insulin resistance. Developing interventions to increase would be useful for new treatment strategies.

History and future perspectives of adipose tissue macrophage biology.

Macrophages contribute to adipose tissue homeostasis; however, they are also thought to be responsible for insulin resistance in obesity. Macrophages, which were oversimplified in past methodologies, have become rather difficult to understand comprehensively as recent developments in research methodology have revealed their diversity. This review highlights recent studies on adipose tissue macrophages, identifies controversial issues that need to be resolved and proposes a scenario for further development of adipose tissue macrophage biology.

Characterization of Diabetic Striatopathy With Repeated Follow-Up Using Multiple Imaging Studies.

Diabetic striatopathy is a rare condition with a prevalence of less than one in 100,000. Herein, we report a case of diabetic striatopathy exacerbated by hyperglycemia and hypoglycemia, with repeated follow-up with multiple imaging studies. This case suggested that putamen neuronal loss and dysfunction, gliosis, and ischemia are associated with diabetic striatopathy pathophysiology.

Isoxanthohumol improves obesity and glucose metabolism via inhibiting intestinal lipid absorption with a bloom of Akkermansia muciniphila in mice.

Objective: Polyphenols have health-promoting effects, such as improving insulin resistance. Isoxanthohumol (IX), a prenylated flavonoid found in beer hops, has been suggested to reduce obesity and insulin resistance; however, the mechanism remains unknown.

Methods: High-fat diet-fed mice were administered IX.

Heterogeneity of adipose tissue-resident macrophages-beyond M1/M2 paradigm.

Adipose tissue-resident macrophages (ATMs) are reported to be important for maintaining adipose tissue remodeling and homeostasis. ATMs were classified for the first time in 2007 into the M1 and M2 types. This theory suggests that in the non-obese adipose tissue, the anti-inflammatory, alternatively activated macrophages (AAMs) predominate, and regulate tissue homeostasis, remodeling, and insulin sensitivity.

Depletion of CD206 M2-like macrophages induces fibro-adipogenic progenitors activation and muscle regeneration.

Muscle regeneration requires the coordination of muscle stem cells, mesenchymal fibro-adipogenic progenitors (FAPs), and macrophages. How macrophages regulate the paracrine secretion of FAPs during the recovery process remains elusive. Herein, we systemically investigated the communication between CD206 M2-like macrophages and FAPs during the recovery process using a transgenic mouse model.

Astaxanthin, a Marine Carotenoid, Maintains the Tolerance and Integrity of Adipose Tissue and Contributes to Its Healthy Functions.

Recently, obesity-induced insulin resistance, type 2 diabetes, and cardiovascular disease have become major social problems. We have previously shown that Astaxanthin (AX), which is a natural antioxidant, significantly ameliorates obesity-induced glucose intolerance and insulin resistance. It is well known that AX is a strong lipophilic antioxidant and has been shown to be beneficial for acute inflammation.

Fate of adipocyte progenitors during adipogenesis in mice fed a high-fat diet.

Objective: Expansion of adipose tissue during obesity through the recruitment of newly generated adipocytes (hyperplasia) is metabolically healthy, whereas that through the enlargement of pre-existing adipocytes (hypertrophy) leads to metabolic complications. Accumulating evidence from genetic fate mapping studies suggests that in animal models receiving a high-fat diet (HFD), only adipocyte progenitors (APs) in gonadal white adipose tissue (gWAT) have proliferative potential. However, the proliferative potential and differentiating capacity of APs in the inguinal WAT (iWAT) of male mice remains controversial.

Gut microbiota, determined by dietary nutrients, drive modification of the plasma lipid profile and insulin resistance.

The gut microbiota metabolizes the nutrients to produce various metabolites that play crucial roles in host metabolism. However, the links between the microbiota established by different nutrients and the microbiota-influenced changes in the plasma lipids remain unclear. Diets rich in cornstarch, fructose, branched chain amino acids, soybean oil (SO), or lard established a unique microbiota and had influence on glucose metabolism, which was partially reproduced by transferring the microbiota.

Astaxanthin stimulates mitochondrial biogenesis in insulin resistant muscle via activation of AMPK pathway.

Background: Skeletal muscle is mainly responsible for insulin-stimulated glucose disposal. Dysfunction in skeletal muscle metabolism especially during obesity contributes to the insulin resistance. Astaxanthin (AX), a natural antioxidant, has been shown to ameliorate hepatic insulin resistance in obese mice.

Peripheral PD1-positive CD4 T-Lymphocyte Count Can Predict Progression-free Survival in Patients With Non-small Cell Lung Cancer Receiving Immune Checkpoint Inhibitor.

Background/aim: Little information is available about the association between peripheral T-lymphocyte expression of programmed cell death protein 1 (PD1) and the efficacy of immune checkpoint inhibitor therapy in patients with non-small cell lung cancer (NSCLC). We analyzed the PD1 and cytotoxic T-lymphocyte associated protein 4 (CTLA4) expression in peripheral blood T-lymphocytes of patients with NSCLC receiving immune checkpoint inhibitor therapy.

Patients And Methods: Patients with NSCLC who were scheduled to receive treatment with immune checkpoint inhibitors were prospectively enrolled in this study between November 2017 and November 2018.

Linkage of CD8 T cell exhaustion with high-fat diet-induced tumourigenesis.

Obesity increases the risk of cancer. Increased levels of hormones (such as oestrogen, insulin, insulin-like growth factor, and leptin), free fatty acid-induced production of reactive oxygen species, an altered intestinal microbiome and chronic inflammation are known to be associated with an increased cancer risk in obese subjects. However, the mechanism underlying the connection between obesity and cancer development remains elusive.

Macrophage-specific hypoxia-inducible factor-1α deletion suppresses the development of liver tumors in high-fat diet-fed obese and diabetic mice.

Aims/introduction: Chronic inflammation of the liver is often observed with obesity or type 2 diabetes. In these pathological conditions, the immunological cells, such as macrophages, play important roles in the development or growth of liver cancer. Recently, it was reported that hypoxia-inducible factor-1α (HIF-1α) is a key molecule for the acquisition of inflammatory M1 polarity of macrophages.

Partial depletion of CD206-positive M2-like macrophages induces proliferation of beige progenitors and enhances browning after cold stimulation.

Beige adipocytes are an inducible form of thermogenic adipocytes that become interspersed within white adipose tissue (WAT) depots in response to cold exposure. Previous studies have shown that type 2 cytokines and M2 macrophages induce cold-induced browning in inguinal WAT (ingWAT) by producing catecholamines. Exactly how the conditional and partial depletion of CD206 M2-like macrophages regulates the cold-induced browning of ingWAT, however, remains unknown.

Publisher Correction: Sirt1 activator induces proangiogenic genes in preadipocytes to rescue insulin resistance in diet-induced obese mice.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper.

Sirt1 activator induces proangiogenic genes in preadipocytes to rescue insulin resistance in diet-induced obese mice.

Sirt1 plays an important role in regulating glucose and lipid metabolism in obese animal models. Impaired adipose tissue angiogenesis in the obese state decreases adipogenesis and thereby contributes to glucose intolerance and lipid metabolism. However, the mechanism by which Sirt1 activation affects obesity-associated impairments in angiogenesis in the adipose tissue is not fully understood.

CD206 M2-like macrophages regulate systemic glucose metabolism by inhibiting proliferation of adipocyte progenitors.

Adipose tissue resident macrophages have important roles in the maintenance of tissue homeostasis and regulate insulin sensitivity for example by secreting pro-inflammatory or anti-inflammatory cytokines. Here, we show that M2-like macrophages in adipose tissue regulate systemic glucose homeostasis by inhibiting adipocyte progenitor proliferation via the CD206/TGFβ signaling pathway. We show that adipose tissue CD206 cells are primarily M2-like macrophages, and ablation of CD206 M2-like macrophages improves systemic insulin sensitivity, which was associated with an increased number of smaller adipocytes.

M2 macrophages in metabolism.

Adipose tissue not only functions as the major energy-storing tissue, but also functions as an endocrine organ that regulates systemic metabolism by releasing various hormones called adipokines. Macrophages play a critical role in maintaining adipocyte health in a lean state and in remodeling during the progression of obesity. Large numbers of classically activated (M1) macrophages accumulate in adipose tissue as adipocytes become larger because of excessive energy conditions, and they adversely affect insulin resistance by triggering local and systemic inflammation.

HIF-1α in Myeloid Cells Promotes Adipose Tissue Remodeling Toward Insulin Resistance.

Adipose tissue hypoxia is an important feature of pathological adipose tissue expansion. Hypoxia-inducible factor-1α (HIF-1α) in adipocytes reportedly induces oxidative stress and fibrosis, rather than neoangiogenesis via vascular endothelial growth factor (VEGF)-A. We previously reported that macrophages in crown-like structures (CLSs) are both hypoxic and inflammatory.