The low-carbohydrate diet and cardiovascular risk factors: Evidence from epidemiologic studies

AimsObesity is an important public health issue because of its high prevalence and concomitant increase in risk of cardiovascular diseases. Low carbohydrate diets are popular for weight loss and weight management but are not recommended in leading guidelines due to the perception that increases in dietary fat intake may lead to an adverse cardiovascular risk profile. To clarify the effects of a low-carbohydrate diet for weight loss on cardiovascular disease risk factors as compared to a low fat diet for weight loss, we systematically reviewed data from randomized controlled clinical trials and large observational studies.Data synthesisWe searched the MEDLINE database (Jan 1966–Nov 2013) to identify studies that examined a low-carbohydrate diet as compared to a low-fat diet for weight loss or the improvement of cardiovascular disease risk factors.ConclusionsRecent randomized controlled trials document that low-carbohydrate diets not only decrease body weight but also improve cardiovascular risk factors. In light of this evidence from randomized controlled trials, dietary guidelines should be re-visited advocating a healthy low carbohydrate dietary pattern as an alternative dietary strategy for the prevention of obesity and cardiovascular disease risk factors.     

Adipocytokine changes caused by low-carbohydrate compared to conventional diets in obesity

Modest weight loss causing a decrease in insulin resistance has been linked to favorable changes in the adipocyte cytokines leptin, adiponectin, and tumor necrosis factor-alpha (TNF-alpha), three emerging risk factors of cardiovascular disease. We previously observed a significant reduction in insulin resistance with weight loss in obese subjects on a low-carbohydrate diet. Based on these previous findings, we hypothesize that a low-carbohydrate diet would be more beneficial in changing leptin, TNF-alpha, and adiponectin than a conventional diet. A total of 75 severely obese (body mass index >/=35 kg/m(2)) subjects were randomized to instruction of 6 months of a low-carbohydrate diet or a conventional calorie-restricted diet. Serum levels of leptin, TNF-alpha, TNF-alpha-soluble receptor 1 (TNF-alpha SR1), and adiponectin were measured at baseline and after 6 months of dietary intervention. Subjects on low-carbohydrate diets experienced a greater decrease in leptin when compared to conventional dieters (p < 0.001). TNF-alpha increased significantly in nondiabetic subjects on conventional vs. low-carbohydrate diets (p = 0.003). Adiponectin and TNF-alpha SR1 change were not significantly different between diets. This is the first study to report the effects of dietary macronutrient alterations on serum adipocytokines in a randomized controlled trial. The greater reduction in insulin resistance and weight on a low-carbohydrate diet, in the short term, translates into greater improvement in leptin but with no significant improvements in TNF-alpha or adiponectin in patients with moderate to severe obesity after 6 months of dietary intervention.     

Atkins and other low-carbohydrate diets: hoax or an effective tool for weight loss?

CONTEXT: The Atkins diet books have sold more than 45 million copies over 40 years, and in the obesity epidemic this diet and accompanying Atkins food products are popular. The diet claims to be effective at producing weight loss despite ad-libitum consumption of fatty meat, butter, and other high-fat dairy products, restricting only the intake of carbohydrates to under 30 g a day. Low-carbohydrate diets have been regarded as fad diets, but recent research questions this view. STARTING POINT: A systematic review of low-carbohydrate diets found that the weight loss achieved is associated with the duration of the diet and restriction of energy intake, but not with restriction of carbohydrates. Two groups have reported longer-term randomised studies that compared instruction in the low-carbohydrate diet with a low-fat calorie-reduced diet in obese patients (N Engl J Med 2003; 348: 2082-90; Ann Intern Med 2004; 140: 778-85). Both trials showed better weight loss on the low-carbohydrate diet after 6 months, but no difference after 12 months. WHERE NEXT?: The apparent paradox that ad-libitum intake of high-fat foods produces weight loss might be due to severe restriction of carbohydrate depleting glycogen stores, leading to excretion of bound water, the ketogenic nature of the diet being appetite suppressing, the high protein-content being highly satiating and reducing spontaneous food intake, or limited food choices leading to decreased energy intake. Long-term studies are needed to measure changes in nutritional status and body composition during the low-carbohydrate diet, and to assess fasting and postprandial cardiovascular risk factors and adverse effects. Without that information, low-carbohydrate diets cannot be recommended.     

Diabetes induces endothelial dysfunction but does not increase neointimal formation in high-fat diet fed C57BL/6J mice

Studies of diabetic vascular disease have traditionally used murine models of type 1 diabetes and genetic models of type 2 diabetes. Because the majority of patients with type 2 diabetes have diet induced obesity, we sought to study the effect of diabetes on arterial disease in a mouse model of diet induced obesity/diabetes. C57Bl/6 mice fed a high-fat diet for 9 weeks developed type 2 diabetes characterized by elevated body weight, hyperglycemia, and hyperinsulinemia. Arteries from diabetic mice exhibited a marked decrease in endothelium-dependent vasodilation, a modest decrease in endothelium independent vasodilation, and an increase in sensitivity to adrenergic vasoconstricting agents. Insulin stimulated protein kinase B (akt) and endothelial nitric oxide synthase (eNOS) phosphorylation were preserved in arteries from diabetic mice; however, eNOS protein dimers were markedly diminished. Arterial nitrotyrosine staining indicated that increased levels of peroxynitrite contributed to eNOS dimer disruption in the diabetic mice. The abnormal vasomotion was not an acute response to the high-fat diet, as short term high-fat diet feeding had no effect on endothelium dependent dilation. A trend toward smaller neointimal lesions was noted in high-fat diet fed mice after femoral artery wire denudation injury. In summary, disrupted eNOS dimer formation rather than impaired insulin mediated eNOS phosphorylation contributed to the endothelial dysfunction in diet induced obese/diabetic mice. The lack of an increase in neointimal formation indicates that additional diabetes associated parameters (such as hyperlipidemia and atherosclerotic vascular disease) may need to be present to increase neointimal formation in this model.     

Obesity and changes in urine albumin/creatinine ratio in patients with type 2 diabetes: The DEMAND Study

Background and aimsObesity is a potential risk factor for renal disease in non-diabetic subjects. It remains unclear whether this also applies to diabetic patients. We investigated whether obesity predicted changes in albumin excretion rate in individuals with type 2 diabetes.Methods and resultsFifty Italian diabetes outpatient clinics enrolled a random sample of 1289 patients. A morning spot urine sample was collected to determine urinary albumin/creatinine ratio (ACR) at baseline and after 1 year from the study initiation. Progression of albumin excretion was defined as a doubling in ACR, while regression was defined as a 50% reduction. Multivariate logistic regression analyses were used to evaluate correlates of these outcomes. Data are expressed as odds ratios (OR) with 95% confidence intervals (CI).The risk of progression increased by 7% (OR = 1.07; 95%CI 1.00–1.15) for every 5-cm increase in waist circumference measured at baseline, and by 17% (OR = 1.17; 95%CI 1.03–1.33) for every one-unit increase in BMI during follow-up. The likelihood of regression was not independently associated with any of the variables investigated. The effect of obesity on progression of ACR was independent of metabolic control, blood pressure, treatment, and baseline level of albumin excretion.ConclusionsWe found a tight link between obesity and changes in albumin excretion in diabetic subjects, suggesting potential benefits of interventions on body weight on end-organ renal damage.     

Contribution of diet to gut microbiota and related host cardiometabolic health: diet-gut interaction in human health

ABSTRACT

Obesity and cardiometabolic diseases in both developed and developing counties in a state of nutrition transition are often related to diet, which also play a major role in shaping human gut microbiota. The human gut harbors diverse microbes that play an essential role in the well-being of their host. Complex interactions between diet and microorganisms may lead to beneficial or detrimental outcomes to host cardiometabolic health. Despite numerous studies using rodent models indicated that high-fat diet may disrupt protective functions of the intestinal barrier and contribute to inflammatory processes, evidence from population-based study is still limited. In our recent study of a 6-month randomized controlled-feeding trial, we showed that high-fat, low-carbohydrate diet was associated with unfavorable changes in gut microbiota, fecal microbial metabolites, and plasma proinflammatory factors in healthy young adults. Here, we provide an overview and extended discussion of our key findings, and outline important future directions.     

The anti-inflammatory agent 5-ASA reduces the level of specific tsRNAs in sperm cells of high-fat fed C57BL/6J mouse sires and improves glucose tolerance in female offspring

IntroductionThe prevalence of obesity and associated comorbidities have increased to epidemic proportions globally. Paternal obesity is an independent risk factor for developing obesity and type 2 diabetes in the following generation, and growing evidence suggests epigenetic inheritance as a mechanism for this predisposition. How and why obesity induces epigenetic changes in sperm cells remain to be clarified in detail. Yet, recent studies show that alterations in sperm content of transfer RNA-derived small RNAs (tsRNAs) can transmit the effects of paternal obesity to offspring. Obesity is closely associated with low-grade chronic inflammation. Thus, we evaluated whether the anti-inflammatory agent 5-aminosalicylic acid (5-ASA) could intervene in the transmission of epigenetic inheritance of paternal obesity by reducing the inflammatory state in obese fathers.MethodsMale C57BL/6JBomTac mice were either fed a high-fat diet or a high-fat diet with 5-ASA for ten weeks before mating. The offspring metabolic phenotype was evaluated, and spermatozoa from sires were isolated for assessment of specific tsRNAs levels.Results5-ASA intervention reduced the levels of Glu-CTC tsRNAs in sperm cells and improved glucose tolerance in female offspring fed a chow diet. Paternal high-fat diet-induced obesity per se had only a moderate impact on the metabolic phenotype of both male and female offspring in our setting.ConclusionThe results indicate that the low-grade inflammatory response associated with obesity may be an important factor in epigenetic inheritance of paternal obesity.     

The Effect of a Low-Carbohydrate,Ketogenic Diet on Nonalcoholic Fatty Liver Disease: A Pilot Study

Nonalcoholic fatty liver disease is an increasingly common condition that may progress to hepatic cirrhosis. This pilot study evaluated the effects of a low-carbohydrate, ketogenic diet on obesity-associated fatty liver disease. Five patients with a mean body mass index of 36.4 kg/m² and biopsy evidence of fatty liver disease were instructed to follow the diet (<20 g/d of carbohydrate) with nutritional supplementation for 6 months. Patients returned for group meetings biweekly for 3 months, then monthly for the second 3 months. The mean weight change was −12.8 kg (range 0 to −25.9 kg). Four of 5 posttreatment liver biopsies showed histologic improvements in steatosis (P=.02) inflammatory grade (P=.02), and fibrosis (P=.07). Six months of a low-carbohydrate, ketogenic diet led to significant weight loss and histologic improvement of fatty liver disease. Further research is into this approach is warranted.     

Hyperlipidemia: forestalling complications in older diabetics

Mild to moderate hypertriglyceridemia is not associated with specific signs or symptoms in either IDDM or NIDDM. However, symptoms of the "chylomicronemia syndrome," including abdominal pain and acute pancreatitis, can occur when poorly controlled diabetes is present in a patient with a familial form of hyperlipidemia. The low-carbohydrate, high-fat diet that was commonly recommended for diabetics during past years may have contributed to the elevated plasma LDL levels in some individuals. Such "diabetic diets" may also have played a role in the predisposition of diabetics toward atherosclerotic complications.     

Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities

There are few studies comparing the effects of low-carbohydrate/high-protein diets with low-fat/high-carbohydrate diets for obesity and cardiovascular disease risk. This systematic review focuses on randomized controlled trials of low-carbohydrate diets compared with low-fat/low-calorie diets. Studies conducted in adult populations with mean or median body mass index of ≥28 kg m⁻² were included. Thirteen electronic databases were searched and randomized controlled trials from January 2000 to March 2007 were evaluated. Trials were included if they lasted at least 6 months and assessed the weight-loss effects of low-carbohydrate diets against low-fat/low-calorie diets. For each study, data were abstracted and checked by two researchers prior to electronic data entry. The computer program Review Manager 4.2.2 was used for the data analysis. Thirteen articles met the inclusion criteria. There were significant differences between the groups for weight, high-density lipoprotein cholesterol, triacylglycerols and systolic blood pressure, favouring the low-carbohydrate diet. There was a higher attrition rate in the low-fat compared with the low-carbohydrate groups suggesting a patient preference for a low-carbohydrate/high-protein approach as opposed to the Public Health preference of a low-fat/high-carbohydrate diet. Evidence from this systematic review demonstrates that low-carbohydrate/high-protein diets are more effective at 6 months and are as effective, if not more, as low-fat diets in reducing weight and cardiovascular disease risk up to 1 year. More evidence and longer-term studies are needed to assess the long-term cardiovascular benefits from the weight loss achieved using these diets.     

Effects and feasibility of a prehabilitation programme incorporating a low-carbohydrate,high-fat dietary approach in patients with type 2 diabetes: A retrospective study

Background and AimsWe performed a retrospective study of diabetic patients undergoing a targeted multimodal prehabilitation programme to assess changes in their diabetic control and functional capacity prior to surgery. As part of the programme, patients were encouraged to follow a low-carbohydrate, high-fat (LCHF) dietary approach. We aimed to assess the feasibility and effects of this programme on our cohort of patients.MethodsFrom 79 patients attending prehabilitation, 17 (13 males, age (median [interquartile range]): 71 [63–79] years) had Type 2 diabetes and none had Type 1. Patients had undergone a targeted multimodal prehabilitation programme prior to surgery, which comprised supervised exercise sessions (aerobic or resistance training), nutritional education (LCHF suggestion, correct protein intake, and avoidance of processed food), psychological support and medical optimization. Weight, body mass index (BMI), glycosylated haemoglobin (HbA1c), fasting glucose, and functional capacity were measured prior to and after prehabilitation. Data were compared with a Wilcoxon signed-rank test.ResultsThere were significant improvements in HbA1c (P = 0.000), fasting glucose (P = 0.006), weight (P = 0.002), and BMI (P = 0.002). There were no significant improvements in functional capacity.ConclusionsWe have shown that in the preoperative period, a targeted multimodal prehabilitation programme incorporating a LCHF diet improves diabetes control in patients with T2D awaiting elective surgery. Our approach is novel as a LCHF diet has not previously been utilized in patients with diabetes within this context. Prospective studies are required in the context of post-operative outcomes.     

The lipoprotein lipase activator, NO-1886, suppresses fat accumulation and insulin resistance in rats fed a high-fat diet

Abstract Aims/hypothesis. Fat balance is critical in the aetiology of obesity and related diseases. Lipoprotein lipase is of major importance in lipid metabolism. The aim of this study was to investigate the long-term effects of the lipoprotein lipase activator, NO-1886, on substrate utilisation, adiposity and insulin action in rats fed a high-fat diet.?Methods. Male, Sprague-Dawley rats were fed for 10 weeks on a chow diet or a high-fat diet with, or without, NO-1886 (50 mg · kg^–1· day^–1). Weight gain, fat accumulation and both hormone-sensitive and lipoprotein, lipase activities were measured. Insulin action was assessed by the euglycaemic hyperinsulinaemic clamp and metabolic rate/substrate utilisation by open-circuit respirometry.?Results. Compared with chow-fed controls, a high-fat diet increased weight gain, an effect lessened by NO-1886 [weight gain (g): chow, 37 ± 3, high-fat, 222 ± 9; high-fat + NO-1886, 109 ± 6, all groups differed p < 0.001]. A similar pattern existed for fat accumulation [visceral fat (g): chow, 35.9 ± 3.2; high-fat, 81.9 ± 6.6; high-fat + NO-1886, 52.3 ± 4.7, p < 0.01 high-fat vs the other groups]. A high-fat diet induced whole-body insulin resistance (clamp glucose infusion rate: 4.8 ± 1.3 mg · kg^–1· min^–1 vs 10.6 ± 1.1 for the chow group, p < 0.01) with NO-1886 lessening this effect (8.3 ± 0.5, p < 0.05 vs high-fat). The 24-h respiratory quotient was lower in the high-fat + NO-1886 group (0.825 ± 0.010) compared with high-fat alone (0.849 ± 0.004, p < 0.05). A high-fat diet increased lipoprotein and hormone-sensitive, lipase activities in epididymal fat, an effect not altered by NO-1886. In myocardium and skeletal muscle a high-fat diet lowered lipoprotein lipase activity, an effect lessened by NO-1886.?Conclusion/interpretation: Lipoprotein lipase activators could have potential benefits for the treatment of obesity by increasing fat utilisation. [Diabetologia (2000) 43: 875–880] Received: 11 January 2000 and in final revised form: 4 April 2000     

The effect of health literacy-based,health belief-constructed education on glycated hemoglobin (HbA1c) in people with type 2 diabetes: A randomized controlled study

AimsAdopting effective self-care behaviors is essential in maintaining optimal glycated hemoglobin (HbA1c) levels. The study aimed to evaluate the effect of health literacy-based, health belief-constructed education and counseling on glycated hemoglobin (HbA1c) in people with type 2 diabetes.MethodsThe parallel-group, randomized controlled study was conducted between June 2019 and March 2020. One hundred and twenty patients were randomized to receive either 12-week health literacy-based group education and phone counseling (intervention, 60 patients) or routine diabetic care (control, 60 patients). The study was completed with 107 patients (54 intervention, 53 control). HbA1c (primary outcome), self-efficacy, perceived susceptibility, severity, barriers, and benefits (secondary outcomes) were evaluated at baseline and six months.ResultsBoth groups had decreases in HbA1c. There was no significant decrease in HbA1c between the intervention and control groups. However, there was a significant improvement in self-efficacy, change in perceived susceptibility, perceived barriers, and perceived benefits in the intervention group. This effect was the same for all patients in the high and low health literacy intervention groups.ConclusionsEducation and counseling based on health literacy levels and framed with health belief constructs change health beliefs, predicting higher engagement and efficacy in disease management activities.Clinical trial numberNCT04677127.     

The role of energy expenditure in the differential weight loss in obese women on low-fat and low-carbohydrate diets

We have recently reported that obese women randomized to a low-carbohydrate diet lost more than twice as much weight as those following a low-fat diet over 6 months. The difference in weight loss was not explained by differences in energy intake because women on the two diets reported similar daily energy consumption. We hypothesized that chronic ingestion of a low-carbohydrate diet increases energy expenditure relative to a low-fat diet and that this accounts for the differential weight loss. To study this question, 50 healthy, moderately obese (body mass index, 33.2 +/- 0.28 kg/m(2)) women were randomized to 4 months of an ad libitum low-carbohydrate diet or an energy-restricted, low-fat diet. Resting energy expenditure (REE) was measured by indirect calorimetry at baseline, 2 months, and 4 months. Physical activity was estimated by pedometers. The thermic effect of food (TEF) in response to low-fat and low-carbohydrate breakfasts was assessed over 5 h in a subset of subjects. Forty women completed the trial. The low-carbohydrate group lost more weight (9.79 +/- 0.71 vs. 6.14 +/- 0.91 kg; P < 0.05) and more body fat (6.20 +/- 0.67 vs. 3.23 +/- 0.67 kg; P < 0.05) than the low-fat group. There were no differences in energy intake between the diet groups as reported on 3-d food records at the conclusion of the study (1422 +/- 73 vs. 1530 +/- 102 kcal; 5954 +/- 306 vs. 6406 +/- 427 kJ). Mean REE in the two groups was comparable at baseline, decreased with weight loss, and did not differ at 2 or 4 months. The low-fat meal caused a greater 5-h increase in TEF than did the low-carbohydrate meal (53 +/- 9 vs. 31 +/- 5 kcal; 222 +/- 38 vs. 130 +/- 21 kJ; P = 0.017). Estimates of physical activity were stable in the dieters during the study and did not differ between groups. These results confirm that short-term weight loss is greater in obese women on a low-carbohydrate diet than in those on a low-fat diet even when reported food intake is similar. The differential weight loss is not explained by differences in REE, TEF, or physical activity and likely reflects underreporting of food consumption by the low-fat dieters.     

Adipose tissue inflammation induced by high-fat diet in obese diabetic mice is prevented by n−3 polyunsaturated fatty acids

Aims/hypothesis Inflammatory alterations in white adipose tissue appear to underlie complications of obesity including diabetes mellitus. Polyunsaturated fatty acids (PUFA), particularly those of the n−3 series, modulate immune responses and may ameliorate insulin sensitivity. In this study, we investigated how PUFA affect white adipose tissue inflammation and gene expression in obese diabetic animals.Materials and methods We treated db/db mice as well as lean non-diabetic mice (db/+) with either low-fat standard diet (LF) or high-fat diets rich in (1) saturated/monounsaturated fatty acids (HF/S), (2) n−6 PUFA (HF/6) and (3) the latter including purified marine n−3 PUFA (HF/3).Results Many genes involved in inflammatory alterations were upregulated in db/db mice on HF/S compared with LF in parallel with phosphorylation of c-Jun N-terminal kinase (JNK). In parallel, adipose tissue infiltration with macrophages was markedly enhanced by HF/S. When compared with HF/S, HF/6 showed only marginal effects on adipose tissue inflammation. However, inclusion of n−3 PUFA in the diet (HF/3) completely prevented macrophage infiltration induced by high-fat diet and changes in inflammatory gene expression, also tending to reduce JNK phosphorylation (p<0.1) in diabetic mice despite unreduced body weight. Moreover, high-fat diets (HF/S, HF/6) downregulated expression and reduced serum concentrations of adiponectin, but this was not the case with n−3 PUFA.Conclusions/interpretation n−3 PUFA prevent adipose tissue inflammation induced by high-fat diet in obese diabetic mice, thereby dissecting obesity from adipose tissue inflammation. These data suggest that beneficial effects of n−3 PUFA on diabetes development could be mediated by their effect on adipose tissue inflammation. Electronic Supplementary Material Supplementary material is available for this article at and is accessible for authorized users.     

Arterial insulin resistance in Yucatan micropigs with diet-induced obesity and metabolic syndrome

AimMetabolic syndrome affects a large proportion of the population and increases cardiovascular disease risk. Because metabolic syndrome often co-exists clinically with atherosclerosis, it is difficult to distinguish the respective contributions of the components to vascular abnormalities. Accordingly, we utilized a porcine dietary model of metabolic syndrome without atherosclerosis to investigate early abnormalities of vascular function and signaling.MethodsThirty-two Yucatan micropigs were fed either a high-fat, high-simple-sugar, high-calorie (HFHS) or standard chow diet (STD) for 6 months. Neither diet contained added cholesterol. Blood pressure and flow-mediated vasodilatation were assessed at baseline and 6 months. Aortas were harvested at 6 months to assess histology, insulin signaling, and endothelial nitric oxide (eNOS) phosphorylation.ResultsHFHS pigs developed characteristics of metabolic syndrome including obesity, dyslipidemia, and insulin resistance, but without histologic evidence of atherosclerosis. Although arterial intima-media thickness did not differ between groups, vascular dysfunction in HFHS was manifest by increased blood pressure and impaired flow-mediated vasodilation of the femoral artery. Compared with STD, aortas from HFHS exhibited increased p85α expression and Ser307 IRS-1 phosphorylation, and blunted insulin-stimulated IRS-1-associated phosphatidylinositol (PI) 3-kinase activity. In the absence of insulin stimulation, aortic Akt Ser473-phosphorylation was greater in HFHS than in STD. With insulin stimulation, Akt phosphorylation increased in STD, but not HFHS. Insulin-induced Ser1177-phosphorylation of eNOS was decreased in HFHS, compared with STD.ConclusionsPigs with metabolic syndrome develop early vascular dysfunction and aortic insulin signaling abnormalities, and could be a useful model for early human vascular abnormalities in this condition.     

Bloqueio de Receptores AT1 Melhora o Desempenho Funcional Miocárdico na Obesidade

BackgroundObesity has been associated with chronic activation of the renin-angiotensin-aldosterone system and with significant changes in cardiac performance.ObjectiveTo assess the impact of a blockade of angiotensin-II receptor type 1 (AT₁receptor) on morphology and on myocardial functional performance in rats with high-fat diet- induced obesity.MethodsWistar rats (n=48) were submitted to control (2.9 kcal/g) or high-fat (3.6 kcal/g) diet for 20 weeks. After the 16^thweek they were divided into four groups: Control (CO), Obese (OB), Control Losartan (CL) and Obese Losartan (OL). CL and OL received losartan (30 mg/kg/day) in drinking water for four weeks. Subsequently, body composition, systolic blood pressure (SBP) and echocardiographic variables were analyzed. Papillary muscle function was assessed at baseline with 2.50 mM calcium concentration ([Ca²⁺]_o) and after inotropic maneuvers: post-pause potentiation (PPP), [Ca²⁺]_oelevation, and during beta-adrenergic stimulation with isoproterenol. Analysis of the results was performed by the Two-Way ANOVA and by the appropriate comparison test. The level of significance was set at 5%.ResultsAlthough SBP change had been not maintained at the end of the experiment, obesity was associated with cardiac hypertrophy and with increased left ventricle posterior wall shortening velocity. In the study of papillary muscles in basal condition, CL showed lower developed tension maximum negative variation velocity (-dT/dt) than CO. The 60s PPP promoted lower -dT/dt and maximum developed tension (DT) in OB and CL compared with CO, and higher relative DT variation and maximum positive variation velocity (+dT/dt) in OL compared with CL and OB. Under 1.5, 2.0, and 2.5mM [Ca²⁺]_o, the OL group showed higher -dT/dt than CL.ConclusionLosartan improves myocardial function in high-fat diet-induced obesity. (Arq Bras Cardiol. 2020;115(1):17-28)     

The role of gut microbiota in human obesity: Recent findings and future perspectives

AimsIn recent years, gut microbiota have gained a growing interest as an environmental factor that may affect the predisposition toward adiposity. In this review, we describe and discuss the research that has focused on the involvement of gut microbiota in human obesity. We also summarize the current knowledge concerning the health effects of the composition of gut microbiota, acquired using the most recent methodological approaches, and the potential influence of gut microbiota on adiposity, as revealed by animal studies.Data synthesisOriginal research studies that were published in English or French until December 2011 were selected through a computer-assisted literature search. The studies conducted to date show that there are differences in the gut microbiota between obese and normal-weight experimental animals. There is also evidence that a high-fat diet may induce changes in gut microbiota in animal models regardless of the presence of obesity. In humans, obesity has been associated with reduced bacterial diversity and an altered representation of bacterial species, but the identified differences are not homogeneous among the studies.ConclusionsThe question remains as to whether changes in the intestinal microbial community are one of the environmental causes of overweight and obesity or if they are a consequence of obesity, specifically of the unbalanced diet that often accompanies the development of excess weight gain. In the future, larger studies on the potential role of intestinal microbiota in human obesity should be conducted at the species level using standardized analytical techniques and taking all of the possible confounding variables into account.     

The long-term effect of low-carbohydrate/high-fat diet on the development of diabetes mellitus in spontaneously diabetic rats

The long-term effect of low-carbohydrate/high-fat diets on the development of diabetes mellitus was studied in Otsuka Long-Evans Tokushima Fatty strain (OLETF) rats. Four groups of spontaneously diabetic (type 2) male rats at 10 weeks of age were pair-fed semi-purified powder diets containing different amounts of carbohydrate (80%, 60%, 40%, 20% of total calories) for 30 weeks. The carbohydrate content was isocalorically substituted for the fat content in the diet. At the onset of experimental feeding (10 weeks of age), an oral glucose tolerance test (OGTT) was normal in each group. After 15 weeks of the test diet feeding there was no significant difference in the glucose tolerance among the 4 groups, although most of the rats were diabetic. The body weight increased with the decrease of the carbohydrate intake and increase of the fat intake (p <0.05), and the difference increased in proportion to age (p<0.05). The severity of diabetes mellitus was also increased along with the lower carbohydrate intake and higher fat intake, when the carbohydrate intake was less than 60% (in energy). On the other hand, there was a significant increase in the 20% group in the postload plasma insulin levels as compared with the other 3 groups at 40 weeks of age. Fasting plasma free fatty acid levels were increased in the lower carbohydrate content groups (20% and 40%) as compared with the higher carbohydrate content groups (60% and 80%) at the end of the experiment. Impairment of insulin secretion may be the cause of glucose intolerance induced by low carbohydrate intake rather than insulin resistance. These findings suggest that low-carbohydrate/high-fat diet aggravates diabetes mellitus in genetically diabetic rats, and that the development of diabetes mellitus is associated with the activation of the glucose-fatty acid cycle.