Exploration of the relationship between household food insecurity and diabetes in Canada.

OBJECTIVE: To determine the household food insecurity (HFI) prevalence in Canadians with diabetes and its relationship with diabetes management, self-care practices, and health status. RESEARCH DESIGN AND METHODS: We analyzed data from Canadians with diabetes aged >or=12 years (n = 6,237) from cycle 3.1 of the Canadian Community Health Survey, a population-based cross-sectional survey conducted in 2005. The HFI prevalence in Canadians with diabetes was compared with that in those without diabetes. The relationships between HFI and management services, self-care practices, and health status were examined for Ontarians with diabetes (n = 2,523). RESULTS: HFI was more prevalent among individuals with diabetes (9.3% [8.2-10.4]) than among those without diabetes (6.8% [6.5-7.0]) and was not associated with diabetes management services but was associated with physical inactivity (odds ratio 1.54 [95% CI 1.10-2.17]), lower fruit and vegetable consumption (0.52 [0.33-0.81]), current smoking (1.71 [1.09-2.69]), unmet health care needs (2.71 [1.74-4.23]), having been an overnight patient (2.08 [1.43-3.04]), having a mood disorder (2.18 [1.54-3.08]), having effects from a stroke (2.39 [1.32-4.32]), lower satisfaction with life (0.28 [0.18-0.43]), self-rated general (0.37 [0.21-0.66]) and mental (0.17 [0.10-0.29]) health, and higher self-perceived stress (2.04 [1.30-3.20]). The odds of HFI were higher for an individual in whom diabetes was diagnosed at age <40 years (3.08 [1.96-4.84]). CONCLUSIONS: HFI prevalence is higher among Canadians with diabetes and is associated with an increased likelihood of unhealthy behaviors, psychological distress, and poorer physical health.

The effects of fat and protein on glycemic responses in nondiabetic humans vary with waist circumference, fasting plasma insulin, and dietary fiber intake.

The effects of protein and fat on glycemic responses have not been studied systematically. Therefore, our aim was to determine the dose-response effects of protein and fat on the glycemic response elicited by 50 g glucose in humans and whether subjects' fasting plasma insulin (FPI) and diet influenced the results. Nondiabetic humans, 10 with FPI < [corrected] or =40 pmol/L and 10 with FPI >40 pmol/L, were studied on 18 occasions after 10 14-h overnight fasts. Subjects consumed 50 g glucose dissolved in 250 mL water plus 0, 5, 10, or 30 g fat and/or 0, 5, 10, or 30 g protein. Each level of fat was tested with each level of protein. Dietary intake was measured using a 3-d food record. Gram per gram, protein reduced glucose responses approximately 2 times more than fat (P < 0.001) with no significant fat x protein interaction (P = 0.051). The effect of protein on glycemic responses was related to waist circumference (WC) (r = -0.56, P = 0.011) and intake of dietary fiber (r = -0.60, P = 0.005) but was unrelated to FPI or other nutrient intakes. The effect of fat on glycemic responses was related to FPI (r = 0.49, P = 0.029) but was unrelated to WC or diet. We conclude that, across the range of 0-30 g, protein and fat reduced glycemic responses independently from each other in a linear, dose-dependent fashion, with protein having approximately 3-times the effect of fat. A large protein effect was associated with high WC and high dietary-fiber intake, whereas a large fat effect was associated with low FPI. These conclusions may not apply to solid meals. Further studies are needed to determine the mechanisms for these effects.

L-rhamnose and lactulose decrease serum triacylglycerols and their rates of synthesis, but do not affect serum cholesterol concentrations in men.

Colonic short-chain fatty acids (SCFA) may affect hepatic lipid metabolism. Lactulose increases colonic acetate production, whereas L-rhamnose increases propionate. To test the effects of oral L-rhamnose and lactulose for 28 d on fasting concentrations and hepatic synthesis of lipids in humans, 18 men were administered 25 g/d of L-rhamnose, lactulose, or d-glucose for 4 wk in a partially randomized crossover design, with blood collected from fasting subjects on the first and last day of each period. Cholesterol and triacylglycerol (TG) synthesis rates were determined using deuterated water uptake rate over the last 24 h of each period. Postprandial blood lipids, and glucose and insulin were assessed in 11 subjects on d 28. Fasting serum cholesterol was unchanged; however, when expressed as a percentage change, TG were decreased, relative to baseline (P < 0.04), by L-rhamnose (-10%) and lactulose (-10%), compared with D-glucose, which increased serum TG (+11%). Net TG-fatty acid (TGFA) synthesis on d 28 was lower with L-rhamnose (2.42 +/- 0.38 g/d) and lactulose (2.62 +/- 0.35 g/d) than with D-glucose (2.96 +/- 0.31 g/d, P < 0.01). We conclude that these results do not support a primary role for propionate in the cholesterol-lowering effect of soluble fiber. However, both lactulose and L-rhamnose lowered serum TG (expressed as a percentage change) and TGFA synthesis, compared with d-glucose, which increased them. Although these data are consistent with inhibition of TGFA synthesis by SCFA, other aspects of the metabolism of these sugars cannot be ruled out as putative agents of their TG-lowering effects.

L-Rhamnose increases serum propionate after long-term supplementation, but lactulose does not raise serum acetate.

BACKGROUND: Acute ingestion of the unabsorbed sugar l-rhamnose in humans raises serum propionate, whereas acute ingestion of lactulose raises serum acetate. It is not known whether short-chain fatty acid concentrations in urine and feces reflect those in blood. OBJECTIVE: The objective was to test the effects of oral l-rhamnose and lactulose for 28 d on acetate and propionate concentrations in serum, urine, and feces. DESIGN: Eleven subjects ingested 25 g l-rhamnose, lactulose, or d-glucose (control) for 28 d in a partially randomized crossover design. One fecal sample, hourly blood samples, and all urine samples were collected over 12 h on the last day of each phase. RESULTS: The increase in serum propionate was greater after l-rhamnose than after lactulose (P < 0.05). The effect of lactulose on serum acetate was not significant, but lactulose raised the acetate:propionate ratio compared with d-glucose or l-rhamnose in serum (P < 0.005) and urine (P < 0.02). Flatulence was significantly greater after lactulose and l-rhamnose than after d-glucose (P < 0.0001), an effect that lasted 4 wk with lactulose but only 1 wk with l-rhamnose. CONCLUSIONS: This study confirmed that l-rhamnose ingestion over 28 d continues to selectively raise serum propionate in humans. Although serum acetate did not increase significantly after lactulose, the serum acetate:propionate ratio was significantly different after l-rhamnose and lactulose, which suggests that these substrates could be used to examine the role of colonic acetate and propionate production in the effect of dietary fiber on lipid metabolism. Changes in the ratio of urinary acetate to propionate reflected those in serum.

L-Rhamnose increases serum propionate in humans.

BACKGROUND: Acetic and propionic acids are produced by colonic bacterial fermentation of unabsorbed carbohydrates and are absorbed into the portal circulation. From there, they travel to the liver, where acetate is a lipogenic substrate and propionate can inhibit lipogenesis. The extent to which peripheral blood short-chain fatty acid concentrations reflect differences in colonic fermentation is uncertain. The unabsorbed sugar lactulose produces mainly acetate when fermented in vitro, whereas L-rhamnose yields propionate. OBJECTIVE: The objective of the study was to ascertain whether ingestion of L-rhamnose and lactulose would have different acute effects on peripheral acetate and propionate concentrations and on breath hydrogen and methane concentrations. DESIGN: Twenty-two subjects were fed 25 g L-rhamnose, lactulose, or glucose on 3 separate occasions in a randomized crossover design. Blood and breath samples were collected hourly for 12 h. RESULTS: Serum propionate was significantly higher with ingestion of L-rhamnose than with that of lactulose or glucose (P < 0.001). The area under the curve for serum acetate was significantly higher with ingestion of lactulose than with that of glucose (P < 0.03). The ratio of serum acetate to propionate was significantly higher with ingestion of lactulose than with that of glucose or L-rhamnose (P < 0.01). Breath hydrogen was significantly higher with ingestion of lactulose than with that of L-rhamnose or glucose (P < 0.0001). CONCLUSIONS: The selective increases in serum acetate and propionate concentrations in humans were obtained by feeding specific fermentable substrates. Presumably, these changes in serum concentrations reflect changes in colonic production. Selective alteration of colonic fermentation products could yield a new mechanism for modifying blood lipids.

Fecal acetate is inversely related to acetate absorption from the human rectum and distal colon.

In humans, colonic bacteria ferment unabsorbed carbohydrates, producing the SCFA acetic, propionic and n-butyric acids. To test for interactions among the SCFA that may affect their absorption, healthy subjects (n = 10) were given 300-mL rectal infusions containing acetate (60 mmol/L), propionate (20 mmol/L) and butyrate (20 mmol/L), alone or in combinations of two or three. The solutions were retained for 30 min, and then subjects voided a sample for SCFA measurement. To examine the relationship between absorption and fecal SCFA concentrations, a fecal sample was collected at the end of the study. The mean percentage of butyrate absorption (30.2 +/- 4.6%) exceeded that of acetate (24.1 +/- 3.7%) (P < 0.05). Absorption tended to be less (P = 0.12) when a SCFA was infused alone (26.7 +/- 4.0%) than when all three were infused (32.0 +/- 5.7%). Bicarbonate concentration was higher after butyrate-containing infusions than after saline. The fecal molar acetate percentage was inversely correlated with the percentage of acetate absorption from the infusion of three SCFA (r = -0.834, P < 0.005). We conclude that there was no combination effect on SCFA absorption, and the chain-length effect suggests passive diffusion as a likely mechanism of absorption. Furthermore, fecal acetate may reflect absorption, rather than production of colonic acetate.

Do colonic short-chain fatty acids contribute to the long-term adaptation of blood lipids in subjects with type 2 diabetes consuming a high-fiber diet?

BACKGROUND: We recently obtained evidence of long-term adaptation of blood lipids to changes in intakes of carbohydrate and fiber in subjects with type 2 diabetes. OBJECTIVE: We determined the effect of increased carbohydrate and fiber intakes on serum short-chain fatty acids (SCFAs) and the relation between changes in serum acetate and changes in blood lipids. DESIGN: Subjects with type 2 diabetes (n = 62) were randomly assigned to receive approximately 10% of energy from low-fiber breakfast cereal (LF diet), high-fiber breakfast cereal (HF diet), or monounsaturated fatty acids (MUFA diet) for 6 mo. RESULTS: Carbohydrate intakes were higher in the LF and HF groups than in the MUFA group (54% compared with 43%), and more fiber was consumed by the HF group (approximately 50 g/d) than by the LF or MUFA group (approximately 23 g/d). Fasting serum SCFAs did not change significantly over the first 3 mo. Between 3 and 6 mo, serum acetate tended (NS) to decrease in the LF group (from 69 +/- 4 to 59 +/- 5 micromol/L) and increase in the HF group (from 100 +/- 18 to 107 +/- 17 micromol/L), with no significant change in the MUFA group. Serum butyrate did not change significantly in the LF or MUFA group but increased in the HF group (from 2.5 +/- 0.5 to 3.1 +/- 0.6 micromol/L; P < 0.001). Changes in serum acetate from 0 to 3 mo were not related to changes in lipids. However, changes in serum acetate from 3 to 6 mo were positively related to changes in the ratio of total to HDL cholesterol (P = 0.041) and in fasting (P = 0.013) and postprandial (P = 0.016) triacylglycerols. CONCLUSIONS: In subjects with type 2 diabetes, changes in serum SCFAs in response to changes in carbohydrate and fiber intakes took many months to occur, and the changes in serum acetate were significantly related to the long-term adaptive changes in blood lipids.