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Using this guide, you can design a low-carb, low-calorie diet that helps you shed weight while controlling your diabetes. --from publisher description.

Objective The present study aims at determining the stability of a popular type 2 diabetes rat model induced by a high-fat diet combined with a low-dose streptozotocin injection. Methods Wistar rats were fed with a high-fat diet for 8 weeks followed by a one-time injection of 25 or 35 mg/kg streptozotocin to induce type 2 diabetes. Then the diabetic rats were fed with regular diet/high-fat diet for 4 weeks. Changes in biochemical parameters were monitored during the 4 weeks. Results All the rats developed more severe dyslipidemia and hepatic dysfunction after streptozotocin injection. The features of 35 mg/kg streptozotocin rats more resembled type 1 diabetes with decreased body weight and blood insulin. Rats with 25 mg/kg streptozotocin followed by normal diet feeding showed normalized blood glucose level and pancreatic structure, indicating that normal diet might help recovery from certain symptoms of type 2 diabetes. In comparison, diabetic rats fed with high-fat diet presented decreased but relatively stable blood glucose level, and this was significantly higher than that of the control group ( P >0.05). Conclusions This model easily recovers with normal diet feeding. A high-fat diet is suggested as the background diet in future pharmacological studies using this model.

In the late 1980s, pediatric endocrinologists at the Children's Hospital in Winnipeg began to notice a new cohort appearing in their clinics for young people with diabetes. Through dozens of interviews, Krotz shows the impact of the disease on the lives of individuals and families, especially in communities far removed from the medical personnel and facilities available in the city.

Background Non-coding genetic variants that influence gene transcription in pancreatic islets play a major role in the susceptibility to type 2 diabetes (T2D), and likely also contribute to type 1 diabetes (T1D) risk. For many loci, however, the mechanisms through which non-coding variants influence diabetes susceptibility are unknown. Results We examine splicing QTLs (sQTLs) in pancreatic islets from 399 human donors and observe that common genetic variation has a widespread influence on the splicing of genes with established roles in islet biology and diabetes. In parallel, we profile expression QTLs (eQTLs) and use transcriptome-wide association as well as genetic co-localization studies to assign islet sQTLs or eQTLs to T2D and T1D susceptibility signals, many of which lack candidate effector genes. This analysis reveals biologically plausible mechanisms, including the association of T2D with an sQTL that creates a nonsense isoform in ERO1B , a regulator of ER-stress and proinsulin biosynthesis. The expanded list of T2D risk effector genes reveals overrepresented pathways, including regulators of G-protein-mediated cAMP production. The analysis of sQTLs also reveals candidate effector genes for T1D susceptibility such as DCLRE1B , a senescence regulator, and lncRNA MEG3 . Conclusions These data expose widespread effects of common genetic variants on RNA splicing in pancreatic islets. The results support a role for splicing variation in diabetes susceptibility, and offer a new set of genetic targets with potential therapeutic benefit.

Multiple sources of burden for youth with type 1 diabetes (T1D) impact key outcomes including quality of life, self‐management, and glycemic control. Professional diabetes organizations recommend diabetes care providers screen for psychosocial and behavioral challenges and implement strategies to support youth with T1D. The purpose of this article is to review the literature and recommend practical strategies medical providers can use for screening and behavioral support for youth with diabetes and their families. As part of their routine medical care, diabetes care providers are well‐positioned to identify and intervene to address emotional distress related to the burdens of living with diabetes. In collaboration with multidisciplinary team members, including psychologists and mental health professionals, medical providers may be able to successfully implement brief behavioral strategies for screening and providing emotional support.

This review offers a comprehensive analysis of the intricate relationship between the gut virome and diabetes, elucidating the mechanisms by which the virome engages with both human cells and the intestinal bacteriome. By examining a decade of scientific literature, we provide a detailed account of the distinct viral variations observed in type 1 diabetes (T1D) and type 2 diabetes (T2D). Our synthesis reveals that the gut virome significantly influences the development of both diabetes types through its interactions, which indirectly modulate immune and inflammatory responses. In T1D, the focus is on eukaryotic viruses that stimulate the host’s immune system, whereas T2D is characterized by a broader spectrum of altered phage diversities. Promisingly, in vitro and animal studies suggest fecal virome transplantation as a potential therapeutic strategy to alleviate symptoms of T2D and obesity. This study pioneers a holistic overview of the gut virome’s role in T1D and T2D, its interplay with host immunity, and the innovative potential of fecal transplantation therapy in clinical diabetes management.

Aims/hypothesis The aims of the study were to evaluate the association between type 2 diabetes and the risk of death from any cancer and specific cancers in East and South Asians. Methods Pooled analyses were conducted of 19 prospective population-based cohorts included in the Asia Cohort Consortium, comprising data from 658,611 East Asians and 112,686 South Asians. HRs were used to compare individuals with diabetes at baseline with those without diabetes for the risk of death from any cancer and from site-specific cancers, including cancers of the oesophagus, stomach, colorectum, colon, rectum, liver, bile duct, pancreas, lung, breast, endometrium, cervix, ovary, prostate, bladder, kidney and thyroid, as well as lymphoma and leukaemia. Results During a mean follow-up of 12.7 years, 37,343 cancer deaths (36,667 in East Asians and 676 in South Asians) were identified. Baseline diabetes status was statistically significantly associated with an increased risk of death from any cancer (HR 1.26; 95% CI 1.21, 1.31). Significant positive associations with diabetes were observed for cancers of the colorectum (HR 1.41; 95% CI 1.26, 1.57), liver (HR 2.05; 95% CI 1.77, 2.38), bile duct (HR 1.41; 95% CI 1.04, 1.92), gallbladder (HR 1.33; 95% CI 1.10, 1.61), pancreas (HR 1.53; 95% CI 1.32, 1.77), breast (HR 1.72; 95% CI 1.34, 2.19), endometrium (HR 2.73; 95% CI 1.53, 4.85), ovary (HR 1.60; 95% CI 1.06, 2.42), prostate (HR 1.41; 95% CI 1.09, 1.82), kidney (HR 1.84; 95% CI 1.28, 2.64) and thyroid (HR 1.99; 95% CI 1.03, 3.86), as well as lymphoma (HR 1.39; 95% CI 1.04, 1.86). Diabetes was not statistically significantly associated with the risk of death from leukaemia and cancers of the bladder, cervix, oesophagus, stomach and lung. Conclusions/interpretation Diabetes was associated with a 26% increased risk of death from any cancer in Asians. The pattern of associations with specific cancers suggests the need for better control (prevention, detection, management) of the growing epidemic of diabetes (as well as obesity), in order to reduce cancer mortality.

•The Danish diet is high in saturated fat and low in fiber, vegetables, fruit, and fish.•Dietary adherence is higher in patients with diabetes than in the general population.•Patients with diabetes consume less sugar and alcohol and more fiber and vegetables. The aim of the present study was to examine dietary habits and adherence to dietary recommendations in adult patients with type 1 diabetes (T1D) and type 2 diabetes (T2D) compared with the general population in Denmark. The study was cross-sectional and included 426 patients with T1D and 348 patients with T2D recruited from an outpatient diabetes clinic in the capital region of Denmark. Dietary habits were assessed by a food frequency questionnaire and compared with dietary data from 2,899 participants without diabetes from the Danish National Survey of Dietary Habits and Physical Activity. Patients with diabetes had a 20-50% lower intake of added sugar and alcohol, and a 10-20% higher intake of fibre and vegetables compared with the general population (p<0.001 for all). Patients with T2D had a 37% lower intake of alcohol compared with T1D (p<0.001). Adherence to dietary recommendations (e.g. fibre, saturated fat, vegetables, fruit and fish) were low in all groups but lowest in the general population. The Danish diet is too high in saturated fat and too low in dietary fibre, vegetable, fruit and fish compared to dietary recommendations in both patients with diabetes and the general population. However, our data demonstrate that patients with diabetes consume a healthier diet compared to the general population: Limiting the intake of added sugar and alcohol, and increasing the intake of vegetables and dietary fibre.

Type 2 diabetes (T2D) is a polygenic and multifactorial complex disease, defined as chronic metabolic disorder. It's a major global health concern with an estimated 463 million adults aged 20–79 years with diabetes and projected to increase up to 700 million by 2045. T2D was reported to be one of the four leading causes of non-communicable disease (NCD) deaths in 2012. Environmental factors play a part in the development of polygenic forms of diabetes. Polygenic forms of diabetes often run-in families. Fortunately, T2D, which accounts for 90–95% of the entire four types of diabetes including, Type 1 diabetes (T1D), T2D, monogenic diabetes syndromes (MGDS), and Gestational diabetes mellitus, can be prevented or delayed through nutrition and lifestyle changes as well as through pharmacologic interventions. Typical symptom of the T2D is high blood glucose levels and comprehensive insulin resistance of the body, producing an impaired glucose tolerance. Impaired glucose tolerance of T2D is accompanied by extensive health complications, including cardiovascular diseases (CVD) that vary in morbidity and mortality among populations. The pathogenesis of T2D varies between populations and/or ethnic groupings and is known to be attributed extremely by genetic components and environmental factors. It is evident that genetic background plays a critical role in determining the host response toward certain environmental conditions, whether or not of developing T2D (susceptibility versus resistant). T2D is considered as a silent disease that can progress for years before its diagnosis. Once T2D is diagnosed, many metabolic malfunctions are observed whether as side effects or as independent comorbidity. Mouse models have been proven to be a powerful tool for mapping genetic factors that underline the susceptibility to T2D development as well its comorbidities. Here, we have conducted a comprehensive search throughout the published data covering the time span from early 1990s till the time of writing this review, for already reported quantitative trait locus (QTL) associated with murine T2D and comorbidities in different mouse models, which contain different genetic backgrounds. Our search has resulted in finding 54 QTLs associated with T2D in addition to 72 QTLs associated with comorbidities associated with the disease. We summarized the genomic locations of these mapped QTLs in graphical formats, so as to show the overlapping positions between of these mapped QTLs, which may suggest that some of these QTLs could be underlined by sharing gene/s. Finally, we reviewed and addressed published reports that show the success of translation of the identified mouse QTLs/genes associated with the disease in humans.

Intermittent as well as prolonged fasting are receiving considerable attention and appear favorable in conditions such as metabolic syndrome, type 2 diabetes, and rheumatic diseases. Fasting for individuals with type 1 diabetes (T1D) is generally considered too risky. However, the ability and possibility to change from carbohydrate- to ketone-based fuel supply might be relevant for individuals with T1D. The aim of this patient-led research was to investigate the feasibility, benefit, and safety of a 7-d multimodal fasting intervention in individuals with T1D. This was a non-randomized controlled pilot study, with 20 participants with T1D and 10 without the disease. Data acquisition took place before, after, and 4 mo after the intervention and daily during intervention. Of the individuals with T1D, 19 finished fasting. A mean β-hydroxybutyrate as representative ketone body increased to 2.8 ± 1.9 mmol/L on day 7; whereas average glucose remained between 4.9 (±1.5) and 7.5 (±2.3) mmol/L (89 ± 27 and 136 ± 40 mg/dL). Mean daily insulin dose was adjusted from 24.4 (3–50) IU on the day before fasting to 7.6 (0–26.7) IU on day 7. Quality of life (WHO-5) normalized from 54 (±4.4) to 68.8 (±15; P = 0.01) after fasting. There was a decrease from before until the follow-up 4 mo later of weight from 77.6 (±20.4) to 76.6 (±20.9) kg (P = 0.023) and for body mass index from 27.68 (±7.04) to 26.74 (±7.15) kg/m2 (P = 0.008). Diastolic blood pressure increased from 69.75 (±11.41) to 75.74 (±8.42) mm Hg (P = 0.028) and stayed in a healthy range on average. Fasting-related side effects were all temporary, and slightly more prevalent in those with type 1 diabetes compared with the reference group. This study demonstrated the feasibility, benefits, and safety aspects of a 7-d fast in adults with T1D. [Display omitted] •No ketoacidosis occurred during 7 d of fasting in a group of 20 individuals with type 1 diabetes.•Change from carbohydrate- to ketone-based fuel is possible for people with type 1 diabetes under stable blood sugar values.•By fasting, body mass index and other symptoms and risk factors may show long-term improvements in adults with type 1 diabetes.•Multimodal 7-d fasting in type 1 diabetes, as a method preferred by many patients, could be proven feasible and might serve as an additional treatment option, when efficacy could be proved within a randomized controlled trial