Obesity is a strong risk factor for the development of CVD, hypertension and type 2 diabetes. The overall goal of the present pilot study was to feed strawberries, in the form of freeze-dried powder, to obese subjects to determine whether dietary strawberries beneficially altered lipid profiles and reduced blood markers of inflammation compared with a control intervention. A total of twenty healthy subjects (thirteen females and seven males) aged between 20 and 50 years with a BMI between 30 and 40 kg/m 2 completed the present 7-week double-blind, randomised, cross-over trial. Each subject received a prepared diet 7 d/week for 7 weeks consisting of approximately 35 % of energy from fat, 20 % protein, 45 % carbohydrate and 14 g fibre. Blood was collected on days 1 and 8 for baseline information. After the first week, subjects were randomly assigned to the strawberry powder (equivalent to four servings of frozen strawberries) or control (strawberry-flavoured) intervention for 3 weeks. For the remaining 3 weeks, subjects crossed over to the opposite intervention. Blood was collected again at the end of weeks 3, 4, 6 and 7. A comprehensive chemistry panel, lipid profile analyses and measurement of inflammatory mediators were performed for each blood draw. A 3-week dietary intervention with strawberry powder reduced plasma concentrations of cholesterol and small HDL-cholesterol particles, and increased LDL particle size in obese subjects (P, 0·05). Dietary strawberry powder reduced risk factors for CVD, stroke and diabetes in obese volunteers, suggesting a potential role for strawberries as a dietary means to decrease obesity-related disease.
We previously reported that severe iron deficiency negatively affects bone microarchitecture. Here we determined whether marginal iron restriction that reflects some human consumption patterns could have similar consequences. Thirty-two weanling female rats were randomly divided into four groups and fed the following diets for 10 weeks: (i) iron-adequate, calcium-adequate (FeA:CaA), (ii) calcium-restricted (FeA:CaR), (iii) iron-restricted (FeR:CaA), and (iv) both calcium- and iron-restricted (FeR:CaR) diets. DEXA analysis revealed that CaR decreased bone mineral density (BMD), and FeR decreased whole-body bone mineral content (BMC). Iron-restricted and calcium-restricted groups had lower BMD than did their adequate counterparts. All treatment-restricted groups had lower BMD in the fourth lumbar (L-4) vertebrae than the FeA:CaA group. Vertebrae BMD was lower in all treatment groups compared to the control group, and for BMC, the CaR groups were lower than the CaA groups and the FeR groups were lower that the FeA groups, and BMC were lower in iron- and calcium-restricted groups. The microarchitecture of the L-4 vertebrae was compromised in FeA:CaR, FeR:CaA, and FeR:CaR: (i) the connectivity density was reduced by FeR and by CaR; and (ii) trabecular number was decreased and trabecular separation was increased by FeR. Cortical thickness of the femur was reduced by both FeR and CaR. Finite element analysis revealed that L-4 vertebrae from the FeR:CaA group had greater internal stress with an applied force than the FeA:CaA group and, thus, would be more likely to break. Chelation of iron in cultured osteoblast cells impaired mineralization but had no impact upon Type I collagen deposition. Iron depletion, similar to that occurring among some human populations, reduced bone strength and microarchitecture based on the in vivo and in vitro results reported here. Impaired mineralization with iron depletion appears to be a possible mechanism for the observed bone abnormalities.
The purpose of the present study was to test the anti-inflammatory and blood glucose (BG)-regulating capacity of strawberries in a mouse model of diet-induced obesity. A total of thirty-six male C57BL/6J mice were randomly divided into four groups (nine mice per group). Mice were fed a low-fat diet (LF, 13 % fat), the LF supplemented with 2·6 % freeze-dried strawberry powder (LFSB), a high-fat diet (HF, 44 % fat) or the HF supplemented with 2·6 % strawberry powder (HFSB). Blood samples were collected to measure BG, inflammation and systemic markers for endocrine function of pancreas and adipose tissue. Splenocytes were harvested at the end of the study and activated with either anti-cluster of differentiation (CD) 3/anti-CD28 antibodies or lipopolysaccharide to test immune responsiveness. The HF increased non-fasted BG, insulin, soluble intracellular adhesion molecule-1, E-selectin, leptin, resistin and plasminogen activator protein-1 (P,0·05). High dietary fat decreased IL-4 production from activated splenocytes (P, 0·05). BG concentrations were lower in the mice supplemented with SB (10·64 mmol/l) compared to the non-supplemented mice (11·37 mmol/l; P¼0·0022). BG values were approximately 6·5 % lower in the supplemented mice. Additionally, SB lowered plasma C-reactive protein in the LFSB group compared to the other three groups (P,0·05). The dietary intake of SB approximated one human serving of strawberries. These results, although modest, support a promising role for dietary strawberries in reducing the risks associated with obesity and diabetes, and regulating the levels of inflammatory markers in non-obese individuals.Key words: Diet-induced obesity: Inflammation: Strawberry powder: Blood glucose Obesity is associated with chronic, low-grade systemic inflammation and increases the risks of developing insulin resistance, type 2 diabetes and CVD (1 -3) . Insulin resistance, a major metabolic factor in obesity and type 2 diabetes, is mediated by attenuation or desensitisation of insulin receptor (IR) signalling by two basic mechanisms: (1) serine phosphorylation of the IR and IR substrate (IRS) proteins and/or (2) dephosphorylation of the activating tyrosine residues of the IR or IRS (4) . Enzymes responsible for the IR-desensitising process include protein kinase B, phosphoinositide-3 kinase, glycogen synthase kinase-3, extracellular signal-regulated kinase, c-Jun N-terminal kinase, IkB kinase and protein tyrosine phosphatase 1B (4,5) . IkB kinase is notable for its role in downstream signalling by inflammatory cytokines through the activation of the transcription factor NF-kB, since chronic inflammation promotes insulin resistance.Dysfunction of the vascular endothelium is involved in the progression of insulin resistance to type 2 diabetes, as well as the development of atherosclerosis (6) . Soluble forms of adhesion molecules such as soluble intracellular adhesion molecule-1 (sICAM-1), E-selectin and soluble vascular adhesion molecule-1 (sVCAM-1) secreted by the vascular endothelium circulate in ...
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